Investigation of the biomechanical properties of the human spinal cord and its connective tissue

Human cadaver spinal cord specimens with and without intact pia mater were subjected to axial deformation over various strain rates. For those specimens with the pia mater intact, the force response to an applied stretch ratio of 1.1 was independent of strain rate over 0.1 s−1 to 10 s−1. Plastic deformation of the specimens was noted when the stretch ratio exceeded 1.06. The neo-Hookean elastic modulus for specimens with intact pia mater was 1.40 MPa. In contrast, the neo-Hookean elastic modulus for specimens with the pia mater incised was 0.09 MPa. These results depict that during axial extension, the pia mater is the load bearing structure. In addition to axial loading, spinal cord specimens with intact pia mater were subjected to subluxation in a custom designed apparatus. The neo-Hookean elastic modulus was determined to be 1.45 MPa in these studies. 35% occlusion of the vertebral canal by the simulated vertebral discs resulted in an axial stretch ratio of 1.025 and no evidence of plastic deformation. In contrast, 100% occlusion resulted in an axial stretch ratio of 1.2 and gross plastic deformation similar to that observed by MRI after acute spinal cord injury. These results suggest that the vertebral canal can be minimally occluded without significantly stretching the spinal cord in the axial direction. A novel mechanism for the interaction between the dentate ligaments and pia mater depicted how motion of the dura mater results in deformation of the spinal cord. Individual axons were traced in fixed human spinal cord specimens using the fluorescent tracer DiI. Results from these studies depicted that axons undulate within the neural substance. A tortuosity coefficient was defined and determined for each axon. This inherent undulation of the axons suggests that the spinal cord can undergo deformation without significantly deforming individual axons. Lastly, a mechanism of spinal cord injury was presented that is capable of predicting a variety of clinical syndromes ranging from transient neurapraxia to quadriplegia. This mechanism and the results described within this thesis can be utilized to refine current biofidelic models of the head-neck complex