Biomechanics and electromyography of a common idiopathic low back disorder

Study Design. In vivo feline preparation groups loaded into lumbar flexion at different magnitudes and an unloaded control group. Objective. To demonstrate that a static, constant load flexion of the lumbar spine results in a complex neuromuscular disorder. Summary of Background Data. Epidemiology suggests that static lumbar flexion is a cause of low back disorders. There is little direct experimental evidence describing the physiologic and biomechanical processes that elicit the disorder. Recent evidence shows that static flexion of the spine under constant displacement results in muscular spasms and a prolonged recovery period. The response of the spine to flexion under constant load of various magnitudes (as opposed to constant displacement) is not known. It was hypothesized that static lumbar flexion under constant load may elicit creep in spinal ligaments, discs, etc., causing microdamage and development of a neuromuscular disorder. Methods. The lumbar spine of the feline was subjected to 20 minutes of constant load static flexion at physiologic load intensities from light to heavy while creep of lumbar viscoelastic tissues and EMG from the multifidus muscles of L3-L4 to L5-L6 were recorded. Recordings were continued over a 7-hour rest period after the static flexion was terminated. Results. Spasms and decreasing reflexive EMG were evident during the loading period, and a transient surge of EMG activity occurred at the beginning of the rest period. A second surge of EMG activity was seen 3-4 hours later. The four components of the neuromuscular disorder were present regardless of the load magnitude. A model was developed to quantify the disorder. Conclusion. A four-component neuromuscular disorder was elicited by a 20-minute constant load static flexion even when very light loads were applied. The disorder was elicited by creep of the viscoelastic tissues, which resulted in spasms and muscular hyperexcitability lasting for >24 hours. Although the disorder was transient, the physiologic and biomechanical principles associated with its development could also explain cumulative trauma disorders.