IN-VITRO MODELLING OF THE COLUMN CORD INTERACTION DURING SPINAL BURST FRACTURES

Abstract

Introduction: Spinal cord injury (SCI) continues to challenge the healthcare and the adjunct social welfare systems. Significant advances have been made in our understanding of the pathological cascade following the initial insult. However, this has yet to be translated into clinically significant treatments and one possible reason for this is that little is known about the actual interaction between the cord and the spinal column at the moment of impact; a factor that is becoming increasingly recognised as important. Burst fractures are a common cause of SCI and are sufficiently well defined to allow significant advances to be made in developing laboratory models of the fracture process. Following on from these advances an in-vitro model of the interaction between the cord and burst fracture fragment was developed and used to perform preliminary experiments to establish those factors that are important in determining the extent of probable cord damage.

Methods: A rig was developed that reliably reproduced a range of fragment-cord impact scenarios previously observed in the development of a model of the burst fracture process. In summary, a simulated bone fragment of mass 7.2 g was fired, transversely, at explanted bovine cord (within 3 hours of slaughter) with a velocity of 2.5, 5.0 or 7.5 ms-1. The cords were mounted in a tensile testing machine using a novel clamping system and held at 8 % strain. A surrogate posterior longitudinal ligament (PLL) was included and simulated in three biomechanically relevant conditions: absent, 0 % strain and 14 % strain. The posterior elements were represented by an anatomically correct surrogate. The impacts were recorded by using either a high speed video camera (4500 frames/s) or a series of fine pressure transducers.

Results: The fragments were recorded to undergo the same occlusion profile as previously reported in the burst fracture model, except that the cord itself reduced the level of maximum occlusion possible. All tests displayed the fragment recoiling following maximum occlusion. The maximum occlusion and the time to this position were found to be significantly dependent on both the fragment velocity and the condition of the PLL. Similar results were observed for peak pressure. One surprising result was that maximum occlusion or time to this event did not change with or without the cord being encased in the dura mater; a structure that is thought to protect the cord from external impacts.

Discussion: The model developed here of the cord-column interaction for the burst fracture produced useful initial insights into the factors that affect the impact on the cord. The PLL has a significant role to play in both reducing the peak pressures and the spreading the energy imparted over a longer period. The model has several areas in which it could be improved and these include 1) the incorporation of the perfusion pressure which tends to hydraulically stiffen the cord and 2) the inclusion of the cerebrospinal fluid, which may operate in unison with the dura in protecting the cord from impacts. Future work includes the incorporation of the CSF into the model, the development of surrogate cords and the generation of computational models using novel programming techniques.