Article Text

Download PDFPDF

Mechanisms of cervical spine injury in rugby union: is it premature to abandon hyperflexion as the main mechanism underpinning injury?
  1. Christopher R Dennison1,2,
  2. Erin M Macri3,4,
  3. Peter A Cripton1,2,3
  1. 1Orthopaedic and Injury Biomechanics Group, Departments of Mechanical Engineering and Orthopaedics, University of British Columbia, Vancouver, Canada
  2. 2International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, Canada
  3. 3Centre for Hip Health and Mobility, University of British Columbia, Vancouver, Canada
  4. 4Department of Experimental Medicine, University of British Columbia, Vancouver, Canada
  1. Correspondence to Dr Peter Cripton, Department of Mechanical Engineering, University of British Columbia, 2054-6250 Applied Science Lane, Vancouver, BC, V6T 1Z4, Canada; cripton{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.


Cervical spine injuries in rugby union have received growing worldwide attention owing to their often catastrophic nature.1,,3 Kuster et al4 considered recent changes in the epidemiology as well as the ex vivo biomechanics literature on cervical spine injury during head-first impacts. Kuster postulated that the majority of catastrophic cervical spine injuries before year 2000 occurred through a hyperflexion mechanism in the scrum and since the year 2000, these injuries have occurred during tackles via an axial compression mechanism and related ‘buckling’ of the cervical spine.

Regulators and other stakeholders in the game continually seek to improve understanding of the scope, true incidence and mechanism of these catastrophic injuries. Ideally, a full comprehension of cervical injury mechanisms occurring during rugby would lead to changes in the game, through rule changes or changes in enforcement and/or player coaching or education, which in turn would reduce the incidence of these injuries.2 Achieving such a full comprehension, however, has been elusive.1,,3 ,5,,9 For example, recent changes to the rules have led to reduced time spent in scrum and have altered scrum engagement, which subsequently have been associated with a reduction in incidence of scrum-related cervical spine injury (an injury primarily involving forward positions and accounting for 37%–51% of cervical spine injuries).5 ,7 ,8 ,10 ,11 These changes have therefore affected the distribution of players who get injured, with increased percentage of these injuries now being sustained by back positions than prior to these rule changes, and up to 57% of cervical injuries are now occurring during tackle.4 ,8 ,9 Despite these changes, understanding of the true mechanism of injury remains controversial.

Best evidence suggests rugby union players worldwide currently suffer cervical spine injury and associated spinal cord injury (SCI) between 0.8 and 13 times per 100 000 players per year.3 ,7 ,9 In South Africa alone, it is estimated that there have been 264 rugby-related SCIs between 1980 and 2007.7 Lifetime costs for a single SCI are estimated at US$2.9 million. SCIs can be fatal, and when they are not, they are associated with loss of motor control, sensation, bowel and bladder control,12 increased risk of unemployment,13 depression,14 ,15 substance abuse,16 suicide17 and divorce.18 Given these economic and personal costs, it is clear that any reduction in the incidence of rugby-related SCI will benefit society and the injured. Reduction of incidence through rugby rule changes requires a clear understanding of cervical spine injury and SCI mechanisms which could result in effective prevention strategies and ultimately a safer game.

Kuster's contention that injury is due to axial compression and associated buckling is based on two factors. First, the majority of injuries currently occur during tackle (rather than scrum) which is more likely to involve axial compression (figures 1 and 2). Second, the types of in vivo injuries seen in rugby union since 2000 (ie, facet dislocations) have been recreated in ex vivo cadaveric work through simulated head-first axial impact that involved spine buckling (figure 2C,D). Kuster argues that these two points seem mutually consistent and support a theory that the mechanism of injury in rugby union is primarily via the head-first impact and buckling mechanism rather than hyperflexion as has been predominantly reported.

Kuster et al's analysis fails to adequately recognise the limitations of ex vivo cadaveric studies in simulating the natural mechanics of the in vivo cervical column, reviews a somewhat limited sample of the ex vivo biomechanical work that has been done in the field of head-first impact and does not incorporate studies focused on the biomechanics of facet joint dislocation occurring with other loading vectors/modes. We outline limitations in the published studies on this topic, limitations specific to the subset of articles reviewed by Kuster and offer an alternative, biomechanical engineering-based perspective to Kuster's on the issue of the mechanisms leading to catastrophic cervical spinal injury in rugby union.

Cervical spine injury biomechanics literature

Conclusively determining injury mechanisms in real-world injuries is fraught with challenges. Determining injury from video replay is difficult because it is rare to capture an injury event on video and, even if video is available, perspective issues often make it difficult to determine the postures, positions and impact configurations accurately. Seminal ex vivo studies have also been performed using video reconstruction, testimony and volunteer motions19 ,20 and anthropomorphic test devices21 to help understand injury in sport. Unfortunately, the gross motions of players' heads, necks and torsos on video prevent indication of the exact time of injury and the complicated motions of the internal osteoligamentous structures.22,,24 Testimonials of injured players may not reliably convey the pathoanatomic mechanisms of injury for reasons including recall bias and shock.22 ,25 Ex vivo biomechanical investigations, however, use whole cadavers26 or cadaveric head and neck complexes27,,31 in simulated head-first impact and document time of injury and motions of osteoligamentous structures using high-speed video, high-speed x-ray and high-speed analog data collection.23 ,27

Most retrospective studies and systematic reviews since the 1970s have sugg- ested hyperflexion of the neck as primary mechanism of osteoligamentous injury in rugby union.5 ,32,,37 Hyperflexion is characterised by forward motion of the head, beyond normal craniocervical range (often with the jaw contacting the torso) as shown in figure 1A during scrum engagement and in figure 2A, and is caused by posterior to anterior forces on the head. This mechanism has been shown, in ex vivo spine investigations to result in facet joint contact and ramping of the superior facet up the inferior facet which results in distraction and flexion of the intervertebral joint and, ultimately, facet dislocation38,,40 and it is clearly present for forward players in the scrum.

Figure 1

(A) Forces during the scrum can force the head and neck into flexion and in some cases lead to hyperflexion (player high-lighted in colour); (B) spear and (C) conventional tackles can result in axial compressive forces on the neck.

Figure 2

(A) Hyperflexion of the head and neck is characterised by posterior to anterior motion with the head coming to rest on the upper torso while the neck assumes the profile shown; (B) Hyperextension is characterised by anterior to posterior motion of the head while the neck assumes the profile shown; and (C) Axial buckling is characterised by superior to inferior motion of the head while the neck assumes a c-shape (first order buckling) or (D) serpentine (2nd order buckling) profile.

Kuster et al challenge hyperflexion as the most common mechanism of injury in rugby union and suggest that axial buckling of the cervical column secondary to head-first impact is more likely Kuster et al.4 Head-first impact is characterised by impact to the top of the head (as shown in figure 1B,C). Axial buckling was first documented by Nightingale's group at Duke University through ex vivo head-first impact experiments and it occurs when the posture of the neck assumes a C-shape (figure 2C) or serpentine profile (figure 2D), caused primarily by axial compressive forces and first order (figure 2C) or higher order (figure 2D) mechanical buckling. More specifically, in C-shape buckling, the lower cervical vertebra exhibit flexion while the remaining upper vertebra exhibit extension and the entire cervical column assumes the C-shaped profile shown by the blue line in figure 2C. In serpentine buckling, the first thoracic and lower cervical levels (ie, C7–6) exhibit flexion, while mid-cervical levels (C5-3) exhibit extension, and the remaining upper cervical vertebra assume flexion such that the entire cervical column assumes a serpentine profile as shown in figure 2D.27

Kuster et al imply that hyperflexion is not the probable cause of injury because bilateral facet dislocations are prevalent in cervical spine injuries in rugby union, but have not been reliably produced in biomechanics studies of cervical spine hyperflexion. Kuster et al cite seminal work by Nightingale's group23 that established the buckling mechanism of injury in the cervical spine. Nightingale's results indicated that osteoligamentous injury occurred between 2 ms and 20 ms after head impact when neck posture was buckled (figure 2C,D) and that hyperflexion (figure 2A) and hyperextension (figure 2B) did not occur until well after injury (after 100 ms).

There is biomechanical literature that contradicts Kuster et al's views. Ivancic et al38 ,39 and Panjabi et al40 have shown that flexion moments combined with axial compression and anterior shear forces (like those during scrum and causing hyperflexion) can result in facet dislocations in the lower cervical spine. In fact, several factors like the angle of head impact, initial neck posture and head constraint are all relevant to cervical spine injury from head-first impact. For example, ex vivo work by Nusholtz et al showed that initial head and neck posture and impact angle can dictate postimpact head and neck displacements (ie, hyperflexion or hyperextension) and injuries.26 Pintar et al30 ,41 ,42 and Liu and Dai43 showed that straightening the cervical spine away from natural lordotic posture prior to dynamic compression resulted in a stiffening of the spine and ultimately clinically relevant compression injuries from C4–C6. Camacho et al44 showed in a computational modelling study that thick surface padding and minimising head to impact surface frictional constraint can reduce risk of cervical spine injury. More recent finite element simulations by Hu et al45 indicate that considerable muscle activation prior to head-first impact (as may occur in a player preparing for a tackle) increases cervical spine injury potential considerably in head-first impact.

While a complete review of all biomechanics literature is beyond the scope of Kuster's analysis, it is worth emphasising that mechanics of cervical spine injury are multifactorial and that there is a range of injury mechanisms, including buckling, in the published studies in this area that are all possible during tackle and scrum in rugby union. There is presently insufficient evidence to clearly establish that neck buckling occurs in vivo in any way that would be similar to the manner in which it occurs ex vivo and, like computational models, ex vivo models must also be considered a model, or imperfect representation, of what occurs in vivo. To quote Dr. Nightingale et al: ‘It should be recognised that passive muscle tone would increase the buckling load and possibly alter the modes of deformation due to the stiffening effects of the muscle itself, and the non-linear stiffening effect of the muscle loads on the ligamentous spine.’46

Kuster's discussion does not include the limitations of biomechanics studies to model real-world head impact and in vivo biomechanics. For example, the authors cite an experimental study by Bauze and Ardran as a study that suggests that compression loading is a more likely cause of injury than is loading during flexion.47 However, there are limitations of this study in the context of Kuster et al's work. More specifically, Bauze and Ardran inserted steel spindles into the spinal canal to isolate the level of dislocation with compressive loads. This experimental configuration clearly does not replicate in vivo loading or constraint conditions of the cervical spine. There is also a considerable body of cervical spine buckling and head-first impact research that has failed to produce clinically observed injuries. For example, the Nightingale study cited as evidence for buckling injury23 in Kuster et al's analysis documents a wide spectrum of injuries but only one out of 11 specimens exhibit facet dislocation while the rest exhibit a spectrum of injuries including a large number of upper cervical spine injuries that are not common in rugby. In another publication, Nightingale et al reported an extended data set that incorporated more specimens and only two of 22 specimens exhibited bilateral facet dislocation.46 Finally, Kuster et al fail to discuss that most specimens used in biomechanics studies are from older populations, which presents obvious limitations in extending the biomechanics literature to explain real-world injury in the young.

Injuries to the in vivo spine: does axial buckling occur and is there a clear connection between buckling and injury?

The axial buckling that has been observed in ex vivo cervical spines during Duke University's head-first impact experiments23 has never been documented in vivo, to our knowledge, and whether injury occurs in the same fashion in vivo as it does ex vivo is an open question. The in vivo cervical spine is surrounded by muscles that, through various activation strategies, offer a context-specific combination of cervical compression, dynamic stability, and global stiffening to balance the head on the neck and to create both movement and stability for rugby play. In contrast, the ex vivo spine is devoid of musculature23 ,46 and is placed in a lordotic posture that may or may not be replicated by players engaged in rugby.

The in vivo rugby studies reviewed by Kuster et al do not adequately support the theory of in vivo buckling of the cervical spine and do not demonstrate a clear connection between buckling and injury type. While using the biomechanics literature to support the concept of buckling, Kuster et al present a table of in vivo studies that predominantly indicate hyperflexion as the mechanism of injury, and it is noted that this includes studies published since the year 2000 (ie, after the change in scrum engagement rules). There is apparent disparity between the mechanisms presented through Kuster's systematic review and the author's decision to advance cervical spine buckling as the predominant injury mode in rugby. What exactly is happening in the in vivo spine during cervical injury remains unclear. Based on the evidence to date, it is premature to abandon the hyperflexion concept of injury as a major contributor to contemporary injury mechanisms in rugby.

Are there other cervical spine pathologies emerging in Rugby Union and if so what can be done about them?

Regardless of the mechanism of injury, adequate care and training of the cervical spine is vital in reducing risk. To begin with, it is important to recognise the nature of the cervical spine of a rugby player. In particular, both radiographs and MRI reveal that degenerative changes (including osteophyte formation and narrowing of canal and/or foramina) begin in rugby players sooner than age-matched controls, potentially increasing the risk of injury during play.48,,50 In addition, important physical attributes differ in and among rugby union players. First, cervical range of motion is reduced in rugby forwards compared to backs, and compared to age- and sex-matched non-rugby athletes.51 ,52 Cervical range of motion decreases in rugby players over the course of a single match.51 ,53 Head and neck proprioception (joint position sense) is reduced in rugby players compared to age- and sex-matched non-rugby athletes and in fact is similar to adults above 65 years or to patients with neck pain.51 ,54 Cervical muscle strength (flexion:extension ratio) is decreased in rugby union forwards compared to backs.52 These findings are similar to those in studies investigating neck injury or neck pain.55,,57 In fact, research regarding the cervical spine and dynamic stability (the ability to actively stabilise the neck during functional movement through neuromotor control) has vastly improved our knowledge of cervical function.58,,63 Unfortunately, there appears to be a lag in dissemination of this knowledge into the rugby literature, with no investigations, to the authors' knowledge, regarding dynamic cervical stability and its role in any contact sport. This suggests a need for more studies investigating the cervical neuromuscular function in rugby players. These studies should investigate whether dynamic stabilisation programmes would benefit players recovering from cervical injury. However, they should also consider whether incorporating such programmes into regular training regimes in asymptomatic players could help maintain cervical function, and subsequently reduce risk of injury (either by delaying the accelerated degenerative changes seen in rugby players, or by improving the ability to prepare for or respond to forceful impacts during play).

In the absence of a clear mechanism of injury, where do we go from here?

Despite uncertainty over in vivo injury mechanisms, there are some practical next steps that rugby administrators, coaches, and players can adopt now. It is paramount to minimise the opportunity for both the hyperflexion injury mode and injurious axial loading in the cervical spine during rugby by the following ways:

  • Controlling the time, configuration and player engagement in the scrum to limit the time players have to produce and experience hyperflexion of the neck (as regulations have been concentrating on since approximately 2000),

  • Regulating and controlling tackles through training, regulation and education to prevent injurious forces on the head by preventing both head-first conventional tackle (figure 1C) and spear tackle (figure 1B). Spear tackle appears to be one of the most dangerous manoeuvres for the cervical spine in any sport or activity. It could be considered an ‘attempted paralysis’ manoeuvre and rugby officials should consider whether current penalisation and rules do enough to prevent it,

  • Minimising head to ground impacts by preventing diving towards the ground during tackle through player education.

In addition to these methods proposed above to minimise injurious head and neck loading, regulators could also consider the following to minimise player predisposition to SCI:

  • Consider screening for osteophyte formation in player populations to prevent exposure of players with already degenerated necks to potentially injurious head and neck loads. As discussed above, osteophytes can predispose players to nerve or spinal cord damage relative to healthy populations,

  • Investigate the potential of cervical neuromuscular training as a component of regular training regimes.

Finally, in parallel with these approaches, there is a clear need to definitively establish the most common mechanisms of cervical spine fracture and spinal cord injury in rugby union in order to prevent these injuries. Gaps in the current epidemiological data could be addressed with more detailed video surveillance and detailed injury reconstructions. Additional cadaveric laboratory studies examining rugby-specific cervical spine injury mechanisms are also warranted.


The authors would like to thank Ms Vicky Earle at UBC IT Creative Media for figure production.


  1. 1.
  2. 2.
  3. 3.
  4. 4.
  5. 5.
  6. 6.
  7. 7.
  8. 8.
  9. 9.
  10. 10.
  11. 11.
  12. 12.
  13. 13.
  14. 14.
  15. 15.
  16. 16.
  17. 17.
  18. 18.
  19. 19.
  20. 20.
  21. 21.
  22. 22.
  23. 23.
  24. 24.
  25. 25.
  26. 26.
  27. 27.
  28. 28.
  29. 29.
  30. 30.
  31. 31.
  32. 32.
  33. 33.
  34. 34.
  35. 35.
  36. 36.
  37. 37.
  38. 38.
  39. 39.
  40. 40.
  41. 41.
  42. 42.
  43. 43.
  44. 44.
  45. 45.
  46. 46.
  47. 47.
  48. 48.
  49. 49.
  50. 50.
  51. 51.
  52. 52.
  53. 53.
  54. 54.
  55. 55.
  56. 56.
  57. 57.
  58. 57.
  59. 58.
  60. 59.
  61. 60.
  62. 61.
  63. 62.
  64. 63.
View Abstract


  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement There are no original data associated with this editorial review, and the manuscript (including previous drafts) has not been shared with anybody else.