Acute repetitive lumbar syndrome: a multi-component insight into the disorder.

Purpose: Repetitive Lumbar Injury (RLI) is common in individuals engaged in long term performance of repetitive occupational/sports activities with the spine. The triggering source of the disorder, tissues involved in the failure and biomechanical, neuromuscular, and biological processes active in the initiation and development of the disorder, are not known. The purpose is, therefore, to test, using in-vivo feline model and healthy human subjects, the hypothesis that RLI due to prolonged exposure to repetitive lumbar flexion-extension is triggered by an acute inflammation in the viscoelastic tissues and is characterized by lingering residual creep, pronounced changes in neuromuscular control and transient changes in lumbar stability. This report, therefore, is a summary of a lengthy research program consisting of multiple projects.

Methods: A series of experimental data was obtained from in-vivo feline groups and normal humans subjected to prolonged cyclic lumbar flexion-extension at high and low loads, high and low velocities, few and many repetitions, as well as short and long in-between rest periods, while recording lumbar displacement and multifidi EMG. Neutrophil and cytokines expression analysis were performed on the dissected feline supraspinous ligaments before loading (control) and 7 h post-loading. A comprehensive, time based model was designed to represent the creep, motor control, tissue biology and stability derived from the experimental data.

Results: Prolonged cyclic loading induced creep in the spine, reduced muscular activity, triggered spasms and reduced stability followed, several hours later, by acute inflammation/tissue degradation, muscular hyperexcitability and hyperstability. Fast movement, high loads, many repetitions and short rest periods, triggered the full disorder, whereas low velocities, low loads, long rest and few repetitions, triggered only minor but statistically significant pro-inflammatory tissue degradation and significantly reduced stability.

Conclusion: Viscoelastic tissue failure via inflammation is the source of RLI and is also the process which governs the mechanical and neuromuscular characteristic symptoms of the disorder. The experimental data validates the hypothesis and provides insights into the development of potential treatments and prevention.