Posted by Matthew Mac Partlin on Friday, June 8, 2012

I've been working away on a project for concussion in motorsport and it seems that, much like the rest of medicine, the more we examine what we think we know, the less we find we really do.

Concussion is a problematic injury in sports in general. It's easy to miss and has the potential to do further harm. Watching a rugby player stumble around the field after a blow to his head makes it easy to see how he could fall over and dislocate a shoulder or break his own nose (again); but the most feared acute injury following a concussion is the Second Impact Syndrome ... or so I thought.

The Second Impact Syndrome (SIS) describes a situation where a player sustains a concussive injury and then, before having fully recovered, receives a second blow to the head. This might occur within minutes to days of the initial injury, however the consequences can be catastrophic, resulting in rapid-onset, diffuse cerebral oedema, an acute rise in intracranial pressure (ICP) and death, in the absence of an alternative structural injury such as a bleed or contusion. The mechanism is unclear and is thought to be related to a metabolic vulnerability during the recovery period. As a result, there are several association and sporting group guidelines advising on how to manage a concussed player in order to avoid this devastating pathology, including:

However, it turns out that the concept of the Second Impact Syndrome is not universally accepted. It has been questioned as a valid clinical entity over the past decade and two recent papers in 2011 [2] and 2012 [3] of the journal Current Sports Medicine Reports (Listed by both Medline and PubMed) pick apart the evidence for this syndrome.

The 2011 paper details flaws in the evidence that led to the identification of diffuse cerebral oedema as a consequence of a second hit. The evidence for its existence is based largely on case reports that lack sufficient detail to be sure about the sequence of events. The majority of case reports come from boxing and American gridiron (American football), where repeated blows to the head are common, so defining which blow was the 'second impact' becomes very tricky and any individual blow may have been sufficient in its own right to cause significant intracranial injury.

Using the National Center for Catastrophic Sport Injury Research database at the University of North Carolina, Randolph identified 50 cases of permanent disability and 38 deaths due to sporting head injuries in American gridiron at all player levels between 1997 and 2006. (The retrospective nature of this data dredging lends itself to criticisms of bias.) He then used some mathematics to estimate a number needed to harm (NNH) of 1 per 205,000 player-seasons for an estimated 1.8 million annual gridiron players, or, for a squad of 100 players 1 such outcome every 2,050 seasons. However, of all of these 88 cases over the 10 years, only one was attributed to acute diffuse cerebral oedema, yielding a NNH of 1 per 18 million player-seasons. That is not a common event by any standards.

So, if acute diffuse cerebral oedema wasn't killing or disabling these players, what was? When Randolph examined all of the reports, he found that in fact players who had poor outcomes following head trauma typically had intracranial bleeds, which only require a single blow, not a second impact, and which may of themselves precipitate cerebral oedema. Furthermore, McCrory et al's 2012 paper highlights the only systematic review of SIS which could find only 17 cases in two papers (published in 1998 and 2001, which he was an author of). Even then, just 5 of these cases actually had a proven second impact. 14 of these cases went for subsequent autopsy, of which 11 had evidence of a structural injury such as an intracranial bleed. Given the frequency of head injury in these contact sports and the apparently rare incidence of acute diffuse cerebral injury, some experts now believe that its occurrence represents a genetic vulnerability and does not require a second impact to precipitate it.

What are the implications of all of these findings? Well, it really calls into question the role of baseline neuropsychiatric testing of players in the pre-season, which is advocated by a number of agencies (with backing from the developers of tests such as ImPACT, the Zurich Consensus group [to which McCrory was a contributor and from which the SCAT2 test was produced] and King-Devick), in order to limit the incidence of a second impact injury. If only one blow to the head is required, then the only way to limit the occurrence of acute diffuse cerebral oedema in sports is to ban all contact sports and maybe identify any genetic susceptibility; both of which are impractical for the moment.

Secondly, does that mean that we write off any intervention and simply accept that head injuries in sport can cause death and disability? Absolutely not. It seems unclear right now how much credence to put into the existence or not of the 'Second Impact Syndrome', but it does seem prudent to continue developments in head injury protection and to pull any competitor who sustains a concussive injury and keep them out of play while still symptomatic. When to allow them to return to play becomes the tricky part. Should there be a time limit or should it depend on symptom/sign resolution and what role does sideline neuropsychiatric testing have to play in this decision? At present, there is no prospective evidence that keeping a competitor out until fully recovered, either clinically or by neuropschiatric testing, leads to a lower incidence of subsequent injury. There is, however, evidence [4] that keeping a player out until fully recovered may actually increase the incidence of subsequent injury.

Motor sport is a little different to gridiron or boxing or any of the other sports that have been used to investigate concussion. An impaired driver can not only injure himself further, but has the potential to cause injury to a co-driver, the other competitors, event officials and spectators. Whatever evidence exists for sports in general, there is even less available to inform decisions for motor sport. So for now, managing suspected head injury at motor sport events will likely require common sense, knowledge of the sport's hazards and good clinical judgement along with backing from the National Sporting Authority (ASN; e.g. CAMS in Australia) and agencies such as the FIA.


  • McCrory P, Meeuwisse W, Johnston K, Dvorak J, Aubry M, Molloy M, et al. Consensus Statement on Concussion in Sport: the 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Br J Sports Med. 2009 May;43 Suppl 1:i76-90
  • Randolph C. Baseline neuropsychological testing in managing sport-related concussion: does it modify risk? Curr Sports Med Rep 2011;10:21–26
  • Second impact syndrome or cerebral swelling after sporting head injury. McCrory P, Davis G, Makdissi M. Curr Sports Med Rep. 2012 Jan-Feb;11(1):21-3.
  • McCrea M, Guskiewicz K, Randolph C, et al. Effects of a symptom-free waiting period on clinical outcome and risk of reinjury after sport-related concussion. Neurosurgery. 2009; 65(5):876Y82; discussion 882Y3.