MECHANISM OF INJURY AND PREVENTION

Our understanding of what happens to the cervical spine during low-velocity, rear-end collisions is limited, despite a wealth of experimental studies on the biomechanics of the cervical spine. 65 Most of these studies focus on the injury mechanisms in severe cervical spine injuries. Mathematical modeling and extrapolation from cadaver, animal and mannequin studies of collisions are of limited value to define thresholds of injury in low-velocity collisions. Studies of human volunteers in controlled conditions cannot be easily extrapolated to real collisions.

For the purposes of this report, the Task Force recommends the study by McConnell et al 61 for its description of the kinematic response of human test subjects to low-velocity, rear-end impacts. This study suggests that a six to eight km/h impact, which subjects the cervical spine to as much as 4.5 Gs, constitutes the threshold for mild cervical strain injury. The test subjects experienced a rapid compression-tension cycle directed axially through the cervical spine as a result of the torso ramping up the seat back. Extreme hyperextension-hyperflexion of the cervical spine, commonly reported in cadaver and mannequin experiments, was not observed. The authors theorize that mild clinical symptoms experienced after low-velocity, rear-end collisions might be due to forces directed axially through the cervical spine, rather than by the classic hyperextension-hyperflexion mechanism. There is a need for more research in this area.

An extensive body of literature on prevention exists and a review of this literature could easily be a subject of a separate Task Force. This literature appears in highly diversified publications, depending on whether one is interested in the pre-collision phase (specialized road safety literature), the collision phase (road safety, engineering and biomechanical literature) or the post-collision phase (medical and trauma care systems literature). Consequently, our best evidence synthesis was deliberately limited to the post-collision phase (see Section 4: Best Evidence Synthesis). The pre-collision and collision phases were addressed by the consensus group.

There is a relative scarcity of studies dealing specifically with whiplash in the prevention literature and the consensus group was forced to extrapolate from the general road safety literature.

Interventions designed to reduce the risk of collision, and therefore, whiplash injuries include:

1) interventions designed to reduce driving while intoxicated, such as automatic licence suspension, 41, 70, 124 enforcement of minimum age for purchase and consumption of alcohol 19, 33, 40, 50, 88, 94, 121 and legal accountability of merchants who sell alcoholic beverages to people who are intoxicated; 41, 66

2) measures designed to decrease the risk for teenagers, such as increasing the legal age for license, 89, 91, 92 graduated access to unaccompanied driving 45, 77, 79 and curfew; 81, 80

3) limiting access to driving for individuals on certain medications or with certain medical conditions; 117

4) vehicle-related interventions, such as improvement in tires, anti-lock brakes, improved visibility and lighting 21, 71, 25 and speed control devices; 22 and

5) interventions related to the road environment, such as widening, improving surfaces, increasing visibility of the road environment, 114, 124 reducing highway speed limits, 32, 90 not allowing right turns on red lights 90 and the elimination of hazardous areas or death traps. 23

Unfortunately, the efficacy of some of the above measures is not certain and none have been studied specifically with whiplash prevention in mind.

With respect to prevention during the collision phase, most studies deal with headrests and seat belts. 13, 51, 74, 75, 107, 110, 118, 119, 120 A headrest should protect the occupant by preventing hyperextension of the neck. However, many headrests are ineffective because of poor design and improper positioning. If the headrest and seat back are composed of materials with different stiffness or deformation/energy absorption characteristics, the energy returned to the occupant's torso and neck after a rear-end collision will differ. Headrests are often covered with slow recovery foam while seat backs often have springs that return energy much faster. If the torso rebounds earlier and faster than the head (differential rebound), cervical extension will be amplified. In other instances, instead of being stopped by the headrest, the head is projected forward. At the time of the collision, the head may be too far forward or too high above the headrest for it to prevent hyperextension. A properly positioned headrest should be located so that the horizontal distance to the head is as small as comfortably possible and its top edge should extend about 70mm vertically above the occupant's eye level. These problems could be avoided if all seats and headrests were made in a single piece, high enough to provide fixed and absorbent support for both the head and torso.

Wearing a seat belt may be a risk factor for whiplash and WAD (see Section 4: Risk). The three-point belt can prevent torso rebound, thus increasing the flexion moment at the cervical spine. Furthermore, the single shoulder restraint may induce rotation of the torso and neck when the unrestrained shoulder moves forward. However, cervical problems from the use of seat belts are minor compared to the morbidity and mortality avoided by their use. Furthermore, we emphasize that there is no evidence that individuals who are exempted from wearing seat belts for medical or professional reasons derive more benefits than disadvantages.