Citation

Chang DG, Tencer AF, Ching RP, Treece B, Senft D, Anderson PA. Spine 1994; 19(8): 973-980.

Affiliation

Harborview Medical Center, University of Washington, Seattle.

Copyright

(Copyright © 1994, Lippincott Williams and Wilkins)

DOI

unavailable

PMID

8009357

Abstract

OF BACKGROUND DATA: Although the extent of injury after cervical spine fracture can be visualized by imaging, the deformations that occur in the spinal canal during injury are unknown. STUDY DESIGN: This study compared spinal canal occlusion and axial length changes occurring during a simulated compressive burst fracture with the residual deformations after the injury. METHODS: Canal occlusion was measured from changes in pressure in a flexible tube with fluid flowing through it, placed in the canal space after removal of the cord in cadaver specimens. To measure canal axial length, cables were fixed in C1 and led through the foramen transversarium from C2-T1, then out through the base, where they were connected to the core rods of linearly variable differential transformers (LVDT). Axial compressive burst fractures were created in each of ten cadaveric cervical spine specimens using a drop-weight, while force, distraction, and occlusion were monitored throughout the injury event. Pre- and post-injury radiographs and computed tomography scans compared transient and post-injury spinal canal geometry changes. RESULTS: In all cases, severe compressive injuries were produced. Three had an extension component in addition to compression of the vertebra and retropulsion of bone into the canal. The mean post-injury axial height loss measured from radiographs was only 35% of that measured transiently (3.1 mm post-injury, compared with 8.9 mm measured transiently), indicating significant recovery of axial height after impact. Post-injury and transient height loss were not significantly correlated (r2 = 0.230, P = 0.16) demonstrating that it is not a good measure of the extent of injury. Similarly, mean post injury canal area was 139% of the minimum area measured during impact, indicating recovery of canal space, and post-injury and transient values were not significantly correlated (r2 = 0.272, P = 0.12). Mean post-injury midsagittal diameter was 269% of the minimum transient diameter and showed a weak but significant correlation (r2 = 0.481, P = 0.03). CONCLUSIONS: Two potential spinal cord injury-causing mechanisms in axial bursting injuries of the cervical spine are occlusion and shortening of the canal. Post-injury radiographic measurements significantly underestimate the actual transient injury that occurs during impact.

Language: en