Study design: A nonlinear finite element study of a lumbar spine with different "patterns" of multilevel intervertebral disc degeneration.
Objective: To determine how different patterns of multilevel disc degeneration influence the biomechanical behavior of the lumbar spine.
Summary of background data: Because of the complex etiology of low back pain, it is often difficult to identify the specific factors that contribute to the symptoms of a particular patient. Disc degeneration is associated with the development of low back pain, but its presence is not always synonymous with symptoms. However, studies have suggested that "patterns" of disc degeneration may provide insight into such pain generation rather than the overall presence of degenerative changes. Specifically, individuals with contiguous multilevel disc degeneration have been shown to exhibit higher presence and severity of low back pain than patients with skipped-level disc degeneration (i.e., healthy discs located in between degenerated discs).
Methods: In this study, the biomechanical differences between these patterns were analyzed using a nonlinear finite element model of the lumbar spine. Thirteen separate "patterns" of disc degeneration were evaluated using the model and simulated under normal physiological loading conditions in each of the primary modes of spinal motion.
Results: The results showed that stresses and forces of the surrounding ligaments, facets, and pedicles at certain vertebral levels of the spine were generally lower in skipped-level disc degeneration cases than in the contiguous multilevel disc degenerations cases even when the skipped level contained more degenerated discs.
Conclusion: To our knowledge, this is the first study to illustrate the biomechanics of specific patterns of disc degeneration of the lumbar spine. Using a multilevel disc degeneration model, our study provides insights as to why various patterns of disc degeneration throughout the lumbar spine may affect motion and soft tissue structures as well that may have bearing in the clinical pathway of pain generation.
Level of evidence: N/A.