In a typical rear-end collision, the occupant’s pelvis, torso, and head are accelerated forward in rapid succession. The large inertia of the head results in a horizontal translation (retraction) of the initially stationary head relative to the forward-accelerating torso, and this motion induces compression, shear, and ultimately tension in the cervical spine. Recent clinical studies have localized the chronic pain of many whiplash patients to the cervical facet joints. Subsequent biomechanical experiments involving both human subjects and cadaveric tissues have shown that injury to the facet capsular ligaments may play a role in the pathoanatomy of whiplash injury.
Whiplash has been difficult to study because its pathoanatomy has remained poorly understood, but the facet joints have been recently isolated as a site of chronic pain in many whiplash-injured people.
Biomechanical studies of whiplash injury have used human subjects, animals, cadavers, and mathematical models to investigate possible mechanisms of whiplash injury. The insights gained from these investigations have often been limited by our ignorance of the tissues responsible for the chronic pain suffered by whiplash patients. Recent clinical research, however, has identified a promising candidate tissue for whiplash injury and has provided a new focus for research into the mechanics of whiplash injury.
An understanding of injury mechanics begins with an appreciation of how individuals respond to the kinds of perturbations that produce whiplash injury. Rear-end collisions, where an occupant’s vehicle is struck from behind and accelerated forward, have been associated with both an increased risk of whiplash injury[1-5] and a higher frequency of multiple symptoms compared to other crash directions. As a result, most biomechanical experiments conducted to investigate whiplash injury have used perturbations that simulate a rear-end collision. Many research groups have studied human subjects exposed to whiplash-like perturbations, and despite numerous differences in the collisions, vehicles, seats, and subjects used by these groups, all have observed a relatively stereotyped response in normally seated subjects. During a whiplash-like perturbation, the pelvis is accelerated forward first. Due to a combination of seat back compliance and occupant posture, acceleration of the upper torso lags behind acceleration of the pelvis. This difference in motion between the pelvis and upper torso produces a small rotation of the torso and results in an initial flexion of the neck (q in the Figure), even though the head is still effectively stationary at this point in the induced kinematic response. As the upper torso accelerates forward relative to the head, a horizontal translation, called retraction, develops between the base of the cervical spine and the head and causes the lower vertebrae of the cervical spine to extend. The horizontal shear stiffness of the upright cervical spine is insufficient to overcome the large translational and rotational inertia of the head, and as a result, the upper cervical segments initially flex. The changing configuration of the vertebrae results in the cervical spine being better able to support horizontal forces, and these forces both accelerate the base of the skull forward and set up a rearward rotation (extension) of the head. The Figure shows that the induced motion between the head and torso precedes the reflexive activation of the neck muscles and that the sternocleidomastoid muscles likely operate to restore upright head posture.
In the presence of a properly positioned head restraint, both the head extension angle (q in the Figure) and the horizontal translation (s in the Figure) between the torso and head (retraction) are arrested and reversed by the combination of an external force applied to the head by the head restraint and internal forces developed by both the ligamentous cervical spine and the reflex contraction of the cervical muscles. If no head restraint is present or if a large gap exists between the back of the head and the head restraint, larger extension and retraction motions occur, and head motion may be arrested and reversed by internal ligamentous and muscle forces alone. The relative positions of the head and head restraint at impact can therefore have a significant influence on the magnitude of the head and neck kinematics, and ultimately on the magnitude of the loads applied to the tissues of the cervical spine. After the initial interaction with the seat back and head restraint, the head and torso rebound forward. Forward torso motion may be limited by a seatbelt, whereas forward motion of the head appears to be controlled by sustained activation of the posterior neck muscles (Figure).
Whiplash injury is a neck injury and therefore loads and displacements developed in the neck are of primary interest in the study of whiplash injury mechanics. Many human subject studies, however, have reported only the peak acceleration of the head relative to an external and fixed reference frame. Since peak head acceleration is often the result of head-restraint impact, these peak values do not necessarily reflect loads developed in the tissues of the neck, and may therefore be unrelated to whiplash injury potential. In the Figure, the kinematics of the head have been computed relative to the joint axis between the C7-T1 vertebra to provide a better indication of the dynamics experienced by the neck rather than the head. The first negative peak in the acceleration trace is the result of forward acceleration of the torso relative to the still-stationary head. This first peak is of considerably more interest in the study of whiplash injury than the later and larger positive acceleration peak, which is governed by the impact between the head and the head restraint. The first negative peak is not observed when only head acceleration is measured—a result that highlights the importance of properly quantifying the relative rather than absolute dynamics of the head.
Cadaveric, animal, and human subject experiments have led investigators to propose various anatomical sites for whiplash injury, including the cervical facet joints, facet capsular ligaments,[10-14] vertebral arteries, dorsal root ganglia,[15,16] craniovertebral junction, and cervical muscles.[18-20] Muscle injury may be responsible for some transient symptoms seen in whiplash-injured patients,[20,21] however of the proposed anatomical sites listed above, only the facet joints have been explicitly linked to chronic whiplash pain. The cervical facet joints have therefore become the focus of recent research aimed at understanding the mechanical basis for chronic whiplash injury.
In the study conducted by Lord and colleagues (1996), chronic whiplash pain was relieved in about 60% of whiplash patients by anesthetizing medial branches of the cervical dorsal rami. Articular branches from these nerves run through the capsular tissues and presumably originate from mechanoreceptors and nociceptors in the capsular tissue. Potential injury sites within the facet joints include fractures of the bony elements, bruising of the synovial folds (menisci), or ruptures or tears of the capsular ligament.[9,25] Bony fractures and facet hemarthroses are not commonly observed in whiplash patients and are therefore more likely related to severe loading. Bruising of the synovial folds is reportedly common after fatal head or chest trauma, and motions of the cervical vertebra consistent with this type of injury have been documented in human subjects during the less severe loading typically associated with whiplash injury. High-speed cineradiography used to examine the intervertebral motion of human subjects exposed to simulated rear-end impacts has shown that the C5 vertebra rotates about a higher point relative to the C6 vertebra during impact tests than during voluntary extension movements. This altered pattern of intervertebral motion resulted in increased distraction of the vertebral bodies anteriorly and resulted in greater compression of the facet joints posteriorly during impact-induced motion than during voluntary movement. Though this altered motion was observed in only four of six subjects, these researchers proposed that the posterior synovial fold might be pinched by posterior compression of the facet joints. This proposed mechanism of injury is promising, and follow-up research that quantifies both the loads applied to the meniscus during whiplash exposures and the loads needed to injure the meniscus is needed to confirm whether this proposed injury mechanism occurs at the loads generated during collisions that produce whiplash injury.
Tears or ruptures to the cervical facet joint capsular ligaments have also been observed under severe loading conditions, and excessive capsular ligament strain has been proposed as a possible mechanism for whiplash injury under minor- to moderate-loading conditions. The facet joint capsules contain fine, unmyelinated nerves that likely have nociceptive function, and distending these ligaments by injection of contrast media has produced whiplash-like pain patterns in normal individuals. Using cadaveric cervical-spine motion segments, the engineering strain in the capsular ligaments under both whiplash-like loads and subsequent loading to failure have recently been measured. Maximum strains in the facet joint capsular ligaments under whiplash-like loads were, on average, half of the maximum strains observed to cause subcatastrophic failures of these ligaments. In two of the 13 specimens tested by these researchers, however, the maximum strains observed in the ligament under whiplash-like loads were larger than those observed at their first subcatastrophic failure. This finding suggested that the neck loads that develop during a low-speed rear-end collisions could injure the facet capsular ligaments of some individuals. Further work is still needed to determine whether the subcatastrophic failures identified in the mechanical response of these tissues correlate with localized ruptures within the capsular ligaments and whether these ruptures, if present, generate pain.
Whiplash injury has proved a difficult injury to study because its pathoanatomy has remained poorly understood. The facet joints have been recently isolated as a site of chronic pain in a large proportion of a whiplash-injured population. Human subject testing has provided the necessary kinematic and kinetic response data needed to conduct mechanical tests of these tissues, and subsequent tissue tests have led to a possible mechanical explanation for whiplash injury. Additional research is needed to complete the link between a seemingly minor vehicle collision and the chronic whiplash symptoms experienced by some individuals. Better understanding of the etiology of whiplash injury will ultimately lead to both improved medical care and improved methods of injury prevention.
Dr Siegmund is co-owner of a consulting firm that conducts technical investigations and provides expert opinions to parties in legal disputes. He has given presentations to plaintiff and defence bar associations and had both his time and expenses paid for by those organizations. He has also conducted contract research for the Insurance Corporation of British Columbia.
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Gunter P. Siegmund, PhD, PEng
Dr Siegmund is a mechanical engineer with a doctorate in biomechanics. He is also a principal of MacInnis Engineering Associates of Richmond, BC. Dr Siegmund has authored several academic papers on the biomechanics of whiplash injury, and his expert opinion has been sought often by both sides of medicolegal issues related to whiplash injury.
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