Researchers and clinicians do not currently use the heterogeneity of the primary mechanism of spinal cord injury (SCI) to tailor treatment strategies because the effects of these distinct patterns of acute mechanical damage on long-term neuropathology have not been fully investigated. Computational modelling of SCI enables the analysis of mechanical forces and deformations within the spinal cord tissue that are not visible experimentally. I created a dynamic, hyperviscoelastic three-dimensional finite element (FE) model of the rat cervical spine and simulated contusion and dislocation SCI mechanisms. I investigated the relationship between maximum principal strain and previously published tissue damage patterns, and compared primary injury patterns between mechanisms.

My model incorporates the spinal cord white and gray matter, dura mater, cerebrospinal fluid, spinal ligaments, intervertebral discs, a rigid indenter and vertebrae, and failure criteria for ligaments and vertebral endplates. High-speed (1 m/s) contusion and dislocation injuries were simulated between vertebral levels C3 and C6 to match previous animal experiments, and average peak maximum principal strains were calculated for several regions at the injury epicentre and at 1 mm intervals from +5 mm rostral to -5 mm caudal to the lesion. I compared average peak principal strains to tissue damage measured previously via axonal permeability to 10 kD fluorescein-dextran (Choo, 2007). Linear regression of tissue damage against peak maximum principal strain for pooled data within white matter regions yields significant (p < 0.0001) correlations that are similar for both contusion (R² = 0.86) and dislocation (R² = 0.54).

With additional simulations of cord contusion injuries at lower injury velocities of 3 and 300 mm/s, I found that current material properties used to model the cord are not biofidelic within this velocity range. By fitting existing experimental cord material testing data and plotting alongside the material properties used in several related models, I further demonstrated the remaining divide between experimental data and computational models.

My model enhances our understanding of the differences in injury patterns between SCI mechanisms, and provides further evidence for the link between principal strain and tissue damage. Furthermore, my results speak to a continued need to test cord material properties at a range of strains and strain rates to better refine cord hyperviscoelastic properties.