A new study1 provides some evidence that the spinal nerves themselves may be injured during whiplash injuries. Researchers found that when pigs were subjected to whiplash extension motions, the spinal ganglion showed microscopic evidence of plasma membrane leakage, while pigs subjected to placebo motions did not. Their research indicates that the spinal column experiences a dramatic pressure pulse during the course of the forced head movement. In one test, the internal pressure in the central nervous system jumped from a baseline of 0 mmHg to -75 mmHg in the first 70 milliseconds of the movement, and then to nearly 100 mmHg by 125 milliseconds. They propose a mechanism of injury:
"Aldman2 predicted that transient pressure changes would occur in the central nervous system during swift extension-flexion motion of the human cervical spine. The spinal canal alters its length and thus its inner volume during this type of movement. This induces alterations of the blood volume of the epidural vein plexa. Venous blood is forced to flow along the spinal canal and through the bridging veins in the intervertebral foramina. When the neck motion becomes rapid, as for instance during whiplash extension motion, so will the flow of vein blood. Pressure gradients will arise due to flow resistance and due to the acceleration of fluid mass. Such pressure gradients are expected to rise over the intervertebral foramina and are likely to add to the load caused by mechanical movements of the tissue inside the foramina. Injuries to the spinal ganglia may thus be a consequence. Such a mechanism for the induction of injury would explain several of the symptoms that are known to be claimed by patients exposed to neck extension trauma (whiplash)..."
Furthermore, the authors also offer a possible explanation of injury mechanisms and whiplash pain:
"Crushing or transection of a peripheral nerve, e.g., the sciatic nerve, results in reactive changes in corresponding spinal ganglia nerve cells (Sunderland3, 1978), with an initial loss and subsequent restoration of their afferent input (Woolf et al.4, 1992). Adaptive as well as abberant patterns of synaptic connections are established in deeper laminae in the dorsal horn of the spinal cord concomitant with the regeneration of the injured peripheral nerve. Tentatively, the whiplash-related changes observed in the spinal ganglion neurons could be sufficient to cause a similar loss and rebuilding of the afferent synaptic connections within the laminae in the posterior horn of the spinal cord. That could contribute to the exacerbated clinical symptoms reported by patients even weeks post-whiplash injury."
