Stephen Mattucci1, Jason Speidel2, Jie Liu3, Matt S Ramer4, Brian K Kwon5, Wolfram Tetzlaff6, Thomas R Oxland7. 1. Orthopaedic and Injury Biomechanics Group, Departments of Orthopaedics and Mechanical Engineering, International Collaboration on Repair Discoveries, University of British Columbia, 818 West 10th Avenue, Vancouver, BC, V5Z 1M9, Canada. Electronic address: mattucci.stephen@gmail.com. 2. Orthopaedic and Injury Biomechanics Group, Departments of Orthopaedics and Mechanical Engineering, International Collaboration on Repair Discoveries, University of British Columbia, 818 West 10th Avenue, Vancouver, BC, V5Z 1M9, Canada. Electronic address: jason.speidel@gmail.com. 3. International Collaboration on Repair Discoveries, University of British Columbia, 818 West 10th Avenue, Vancouver, BC, V5Z 1M9, Canada. Electronic address: jliu@icord.com. 4. International Collaboration on Repair Discoveries, University of British Columbia, 818 West 10th Avenue, Vancouver, BC, V5Z 1M9, Canada. Electronic address: ramer@icord.org. 5. International Collaboration on Repair Discoveries, University of British Columbia, 818 West 10th Avenue, Vancouver, BC, V5Z 1M9, Canada. Electronic address: brian.kwon@ubc.ca. 6. International Collaboration on Repair Discoveries, University of British Columbia, 818 West 10th Avenue, Vancouver, BC, V5Z 1M9, Canada. Electronic address: tetzlaff@icord.org. 7. Orthopaedic and Injury Biomechanics Group, Departments of Orthopaedics and Mechanical Engineering, International Collaboration on Repair Discoveries, University of British Columbia, 818 West 10th Avenue, Vancouver, BC, V5Z 1M9, Canada. Electronic address: toxland@icord.org.
Abstract
BACKGROUND: Preclinical spinal cord injury models do not represent the wide range of biomechanical factors seen in human injuries, such as spinal level, injury mechanism, velocity of spinal cord impact, and residual compression. These factors may be responsible for differences observed between experimental and clinical study results, especially related to the controversial issue of timing of surgical decompression. NEW METHOD: Somatosensory Evoked Potentials were used to: a) characterize residual compression depths in a dislocation model, and b) evaluate the physiological effect of whether or not the spinal cord was decompressed following the initial injury, prior to the application of residual compression. Modifications to vertebral clamps and the development of a novel surgical frame allowed us to conduct surgical and injury procedures in a controlled manner without the risk of additional damage to the spinal cord. Behavioural outcomes were evaluated following varying dislocation displacements, in addition to the survivability of 4 h of residual compression following a traumatic injury. RESULTS: Residual compression immediately following the initial dislocation demonstrated significantly different electrophysiological response compared to when the residual compression was delayed. COMPARISON WITH EXISTING METHOD: There are currently no other residual compression models that utilize a dislocation injury mechanism. Many residual compression studies have demonstrated the effectiveness of early decompression, however the compression of the spinal cord is often not representative of clinical traumatic injuries. Preclinical studies typically model residual compression using a sustained force through quasi-static application, when human injuries often occur at high velocities, followed by a sustained displacement occlusion of the spinal canal. CONCLUSIONS: This study has validated several novel procedural approaches and injury parameters, and provided critical details to implement in the development of a traumatic cervical dislocation SCI model with residual compression.
BACKGROUND: Preclinical spinal cord injury models do not represent the wide range of biomechanical factors seen in human injuries, such as spinal level, injury mechanism, velocity of spinal cord impact, and residual compression. These factors may be responsible for differences observed between experimental and clinical study results, especially related to the controversial issue of timing of surgical decompression. NEW METHOD: Somatosensory Evoked Potentials were used to: a) characterize residual compression depths in a dislocation model, and b) evaluate the physiological effect of whether or not the spinal cord was decompressed following the initial injury, prior to the application of residual compression. Modifications to vertebral clamps and the development of a novel surgical frame allowed us to conduct surgical and injury procedures in a controlled manner without the risk of additional damage to the spinal cord. Behavioural outcomes were evaluated following varying dislocation displacements, in addition to the survivability of 4 h of residual compression following a traumatic injury. RESULTS: Residual compression immediately following the initial dislocation demonstrated significantly different electrophysiological response compared to when the residual compression was delayed. COMPARISON WITH EXISTING METHOD: There are currently no other residual compression models that utilize a dislocation injury mechanism. Many residual compression studies have demonstrated the effectiveness of early decompression, however the compression of the spinal cord is often not representative of clinical traumatic injuries. Preclinical studies typically model residual compression using a sustained force through quasi-static application, when human injuries often occur at high velocities, followed by a sustained displacement occlusion of the spinal canal. CONCLUSIONS: This study has validated several novel procedural approaches and injury parameters, and provided critical details to implement in the development of a traumatic cervical dislocation SCI model with residual compression.