Compressive preload reduces segmental flexion instability after progressive destabilization of the lumbar spine.

STUDY DESIGN: Biomechanical human cadaveric study. OBJECTIVE: We hypothesized that increasing compressive preload will reduce the segmental instability after nucleotomy, posterior ligament resection, and decompressive surgery. SUMMARY OF BACKGROUND DATA: The human spine experiences significant compressive preloads in vivo due to spinal musculature and gravity. Although the effect of destabilization procedures on spinal motion has been studied, the effect of compressive preload on the motion response of destabilized, multisegment lumbar spines has not been reported. METHODS: Eight human cadaveric spines (L1-sacrum, 51.4 ± 14.1 yr) were tested intact, after L4-L5 nucleotomy, after interspinous and supraspinous ligaments transection, and after midline decompression (bilateral laminotomy, partial medial facetectomy, and foraminotomy). Specimens were loaded in flexion (8 Nm) and extension (6 Nm) under 0-N, 200-N, and 400-N compressive follower preload. L4-L5 range of motion (ROM) and flexion stiffness in the high-flexibility zone were analyzed using repeated-measures analysis of variance and multiple comparisons with the Bonferroni correction. RESULTS: With a fixed set of loading conditions, a progressive increase in segmental ROM along with expansion of the high-flexibility zone (decrease of flexion stiffness) was noted with serial destabilizations. Application of increasing compressive preload did not substantially change segmental ROM, but did significantly increase the segmental stiffness in the high-flexibility zone. In the most destabilized condition, 400-N preload did not return the segmental stiffness to intact levels. CONCLUSION: Anatomical alterations representing degenerative and iatrogenic instabilities are associated with significant increases in segmental ROM and decreased segmental stiffness. Although application of compressive preload, mimicking the effect of increased axial muscular activity, significantly increased the segmental stiffness, it was not restored to intact levels; thereby suggesting that core strengthening alone may not compensate for the loss of structural stability associated with midline surgical decompression. This suggests that there may be a role for surgical implants or interventions that specifically increase flexion stiffness and limit flexion ROM to counteract the iatrogenic instability resulting from surgical decompression. LEVEL OF EVIDENCE: N/A.