Slow compression spinal cord injuries occur when the spinal canal narrows, the result of infective, degenerative, or oncologic growth within the spine. The narrowed spinal canal and transversely compresses the spinal cord. Strain magnitude, strain rate, axon location, axon size, and the local tissue stress state have been suggested to contribute to primary cellular injury within the white matter. The objective of this thesis was to use a combined computational and experimental approach to investigate the mechanism of slow compression primary cellular injury.
Strips of guinea pig spinal cord white matter were transversely compressed at a quasi-static rate of 0.05 mm/s to quantify the tissue's force-deformation response. A plane strain finite element model (FEM) was developed using the compressible form of the isotropic Mooney-Rivlin hyperelastic strain energy function. Material parameters were found using inverse finite element analysis; the parameters were iterated within the FEM until the model's force-deformation response converged to the experimental response.
Strips of guinea pig spinal cord white matter were uniaxially elongated at a quasi-static rate of 0.05 mm/s. The isotropic Mooney-Rivlin hyperelastic strain energy function was unable to predict the stress-stretch response measured during uniaxial elongation. A transversely isotropic form of the Mooney-Rivlin hyperelastic strain energy function was proposed to describe spinal cord white matter mechanics in both transverse compression and uniaxial elongation.
To fully mechanically characterize the guinea pig spinal cord white matter, time-and rate-dependence was investigated. Tissues were transversely compressed and uniaxially elongated at a rate of 5 mm/s. The Mooney-Rivlin hyperelastic strain energy function was again augmented in order to predict the higher rate force-deformation response, given the quasi-static force-deformation response. Stress relaxation experiments were conducted on strips of guinea pig spinal cord white matter. A two-element Maxwell model was used to characterize the tissue relaxation response.
Finally, stresses and strains generated during quasi-static transverse compression were correlated with in vitro cellular damage. Permeabilized axons were counted using a horseradish peroxidase (HRP) exclusion test. Single regression analyses yielded significant correlations between the dependent variable (HRP uptake density) and the von Mises stress, the in-plane normal stresses, the first and third principal stresses, in-plane shear strains, and the first and third principal strains.
This work was the first to quantify the stress and strain contours developed when the spinal cord white matter is transversely compressed.
