AMERICAN SOCIETY OF BIOMECHANICS Presented at the Twenty-First Annual Meeting of the American Society of Biomechanics Clemson University, South Carolina September 24-27, 1997

Whiplash has been loosely defined as an acceleration injury and most commonly involves an unaware victim in a stationary vehicle being struck from behind. Resulting symptoms, including neck pain, dizziness, and headaches, are non-specific and are reported up to months or years after accidents. Whiplash investigations have ranged from reviews of clinical data to a number of different biomechanical laboratory approaches. The relatively recent Quebec Task Force on Whiplash-Associated Disorders found the need for further biomechanical studies.

Several attempts have been made to define the mechanism of whiplash injuries. A better understanding of injury mechanism will help in injury prevention, diagnosis and treatment. MacNab, realizing the difficulties of clinical studies, turned to experimental trauma of anesthetized monkeys. He found a predominance of anterior element injuries. He hypothesized that it is the hyper-extension of the cervical spine that caused the injuries. Based upon the MacNab theory of hyper-extension as the injury mechanism in whiplash, the head-restraint was designed to prevent neck injuries in rear-end collisions by blocking the hyper-extension of the neck. Although the head-restraint has decreased the injuries, it did not eliminate them. In a study from Sweden, Nygren and co-workers found only a 20% decrease in neck injuries after the introduction of the head-restraint. This would suggest that the hyper-extension injury mechanism, needs to be re-examined.

We hypothesized that there is another injury mechanism, different from the hyper-extension. The goals of our research were: to quantitatively document the intervertebral rotations during experimental whiplash trauma; to quantify the functional injuries to each intervertebral level after the trauma; to image the actual injuries that occurred; and, based upon the findings, to propose an injury mechanism for whiplash trauma.

Eight fresh cadaveric cervical spine specimens including the occiput were used. Functional radiographs and multidirectional flexibility studies documented and quantified mechanical properties of the specimens. Each specimen was provided with a metal head surrogate, and was subjected to simulated whiplash trauma, starting with sled acceleration of 2.5g and ending with 10.5g, in 2g increments (FIGURE 1). During the trauma the specimen was filmed at high speed. Head rotation and translations were recorded by attached potentionmeters. The entire experiment was conducted via a computer. The functional radiographs and multi-directional flexibility tests were repeated after each trauma to quantify the injury. Finally, the injury was visualized by CT-scan, MRI and cryomicrotomy.

Our findings did not support the hyper-extension hypothesis of whiplash injury mechanism. We found distinct bi-phasic kinematic response of the cervical spine to whiplash trauma. In the first phase (50-75ms after the impact), the spine formed an S-shaped curve with flexion at the upper levels and hyper-extension at the lower levels (FIGURE 2). In the second phase (starting at 100-125ms), all levels of the cervical spine were extended but within the physiological limits. The occurrence of anterior injuries in the lower levels in the first phase was confirmed by functional radiography, flexibility test and imaging modalities. Based upon the experimental findings, we propose a new hypothesis: the lower cervical spine is injured when the spine forms an S-shaped curve, significantly before the neck is fully extended; and the full extension of the neck does not cause cervical spine injuries.