Abstract

Spinal cord injury (SCI) can induce prolonged spinal cord compression that may result in a reduction of local tissue perfusion, progressive ischemia, and potentially irreversible tissue necrosis. Due to the combination of risk factors and the varied presentation of symptoms, the appropriate method and time course for clinical intervention following SCI are not always evident. In this study, a three-dimensional finite element fluid-structure interaction model of the cervical spinal cord was developed to examine how traditionally sub-clinical compressive mechanical loads impact spinal arterial blood flow. The spinal cord and surrounding dura mater were modeled as linear elastic, isotropic, and incompressible solids, while blood was modeled as a single-phased, incompressible Newtonian fluid. Simulation results indicate that anterior, posterior, and anteroposterior compressions of the cervical spinal cord have significantly different ischemic potentials, with prediction that the posterior component of loading elevates patient risk due to the concomitant reduction of blood flow in the arterial branches. Conversely, anterior loading compromises flow through the anterior spinal artery but minimally impacts branch flow rates. The findings of this study provide novel insight into how sub-clinical spinal cord compression could give rise to certain disease states, and suggest a need to monitor spinal artery perfusion following even mild compressive loading.

Highlights

  • The incidence of spinal cord injury (SCI) in the United States is approximately 12,000 individuals annually, with causes including various forms of trauma and non-traumatic diseases [1]

  • Both primary and secondary injury mechanisms contribute to progressive spinal cord ischemia, which can cause necrosis and irreversible tissue damage if perfusion falls below a critical level, or vascular threshold [6]

  • The geometry consisted of a 1.5 cm segment of the anterior spinal artery (ASA), cervical spinal cord, cerebral spinal fluid (CSF) region, dura mater, and five arterial branches (L1, L2, L3, R1, and R2) that protrude into the spinal cord (Fig. 1)

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Summary

Introduction

The incidence of spinal cord injury (SCI) in the United States is approximately 12,000 individuals annually, with causes including various forms of trauma and non-traumatic diseases [1]. Anteroposterior compression is observed in facet dislocation without vertebral dislocation (perched or jumped facets with no injury to anterior or posterior longitudinal ligaments) and posteriorly located epidural masses (tumor, abscess, hematoma etc.). Secondary injury is attributed to disruption of the blood-spinal cord barrier, the generation of an inflammatory response, and local biochemical changes, which together compromise tissue health and neurological function over time [3,5]. Both primary and secondary injury mechanisms contribute to progressive spinal cord ischemia, which can cause necrosis and irreversible tissue damage if perfusion falls below a critical level, or vascular threshold [6]. Ischemia must be treated in a time-sensitive manner, with evidence that rapid restoration of blood flow may improve patient outcomes [7]

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