Abstract

The primary injury phase of traumatic spinal cord injury (SCI) was investigated using a novel compression injury model. Ventral white matter from adult guinea pigs was crushed to 25%, 50%, 70%, and 90% ex vivo. During compression, the physical deformation, applied force and the compound action potentials (CAP) were simultaneously recorded. In addition, axonal membrane continuity was analyzed with a horseradish peroxidase (HRP) exclusion assay. Experimental results showed both a CAP decrease and increased HRP uptake as a function of increased compression. The percent CAP reduction was also consistent to the percent HRP uptake, which implies that either metric could be used to assess acute axon damage. Analysis of the HRP stained axon distribution demonstrated a gradient of damage, with the highest levels of staining near the gray matter. The patterns of axon damage revealed by histology also coincided with higher levels of von Mises stress, which were predicted with a recently developed finite element model of ventral white matter. Numerical values obtained from the finite element model suggest stress magnitudes near 2 kPa are required to initiate anatomical tissue injury. We believe that data from this study could further elucidate the deformation-function relationship in acute spinal cord injury.

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