Abstract
Fracture-dislocation is one of the most common causes of spinal cord injury (SCI) in human adults, yet it is not widely studied experimentally. Clinical studies have found that anterior fracture-dislocation occurs more commonly and produces greater neurological deficit than lateral fracture-dislocation. However, the effect of loading direction on SCI neuropathology has not been investigated experimentally and the reasons behind these clinical differences are not known. Thoracolumbar vertebrae T12–L1 of anaesthetized rats were dislocated anteriorly or laterally by 9 mm at 220 mm/sec. Spinal cord sections from animals euthanized at 1, 3, and 6 h post-injury, were stained with hematoxylin and eosin (H&E) to detect hemorrhage, the pathologic accumulation of β–amyloid precursor protein (βAPP) in white matter axons, and degenerating neurons (Fluoro-Jade and loss of NeuN) in the gray matter. The vertebral fracture load and maximum load were similar for both directions of dislocation; however, vertebral fracture occurred at 4.3 mm (±1.5 mm SD) during anterior dislocation compared to 1.1 mm (±0.7 mm SD) during lateral dislocation (p < 0.001). βAPP accumulation and reduction of NeuN immunoreactivity (IR) were greatest along a diagonal band across the spinal cord angled at 45 degrees to the direction of loading (in different planes for each loading direction). Hemorrhage volume (p < 0.05), βAPP-IR, and reduction of NeuN-IR (p < 0.05 in ventral horns) were more pronounced following anterior dislocation. In addition, there was a different spatial distribution of axonal damage for each direction of dislocation. The findings of this study may explain the greater severity of anterior fracture-dislocation observed clinically and reinforces the need to experimentally model differing human SCIs.