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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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Object The correlations between functional deficits, the magnitude of compression, and the role of sustained compression during traumatic spinal cord injury remain largely unknown. Thus, the functional outcome of this type of injury with or without surgical intervention is rather unpredictable. To elucidate how severity and duration of compression affect cord function, the authors have developed a method to study electrophysiological characteristics and axonal membrane damage in white matter from guinea pig spinal cord. Methods Ventral white matter strips isolated from adult guinea pigs were compressed by a compression rod at a level of either 60 or 80% and held briefly, for 30 minutes, or for 60 minutes. In half the experimental groups, a decompression phase consisting of probe withdrawal and 30 minutes of recovery was also applied. For all cord samples, functional response was continuously monitored through compound action potential (CAP) recording. In addition, axonal membrane damage was assessed by a horseradish peroxidase (HRP) exclusion assay. Results After 30 minutes of sustained compression at levels of 60 or 80%, a spinal cord decompression procedure caused a significant CAP recovery, with specimens reaching 97.5 ± 6.84% (p < 0.05) and 56.2 ± 6.14% (p < 0.05) of preinjury amplitude, respectively. After 60 minutes of compression, the amount of CAP recovery following the decompression stage was only 65.5 ± 9.33% for 60% compression (p < 0.05) and 29.8 ± 6.31% for 80% compression (p < 0.05). Unlike the CAP response, HRP uptake did not increase during sustained compression, and the data showed that HRP staining was primarily time dependent. Conclusions The degree of axonal membrane damage is not exacerbated during sustained compression. However, the electrical conductivity of the cord white matter weakens throughout the duration of compression. Therefore, decompression is a viable procedure for preservation of neurological function following compressive injury.

Slow compression spinal cord injuries occur when the spinal canal narrows, the consequence of degenerative, infective, or oncologic legion growth, and exerts pressure throughout the spinal cord. Transverse tissue compression results in an amalgamation of mechanical insults at the cellular level [1]. However, the mechanism of cellular injury has yet to be elucidated. We have recently developed a hyperelastic, isotropic plane strain finite element model (FEM) of the guinea pig spinal cord white matter response to transverse compression based on force-deformation curves measured in vitro. The strongest correlation with in vitro axonal injury density was the combination of the in-plane shear stress with the in- and out-of-plane normal stresses quantified using the FEM [2]. However, we hypothesize that the guinea pig spinal cord white matter is a transversely isotropic material. Material anisotropy must be incorporated into the FEM to achieve enhanced model accuracy, specifically, the prediction of axial stresses within the spinal cord parenchyma during transverse tissue compression. Therefore, the objective of the present study was to propose a compressible, transversely isotropic, hyperelastic constitutive model of the guinea pig spinal cord white matter.