Neuromuscular dysfunction elicited by cyclic lumbar flexion.

An attempt was made to develop an in vivo model that could explain the neurophysiological and biomechanical processes active in the development of the idiopathic low back disorder common in workers who perform repetitive lifting tasks in industry. Passive cyclic flexion of the feline lumbar spine at 0.1 HZ for 20 min resulted in creep of the supraspinous ligament and other lumbar viscoelastic tissues as well as spasms superimposed on a decreasing electromyogram (EMG) elicited reflexly from the multifidus muscles. Rest for 7 h did not allow full recovery of the viscoelastic creep; the multifidus EMG gradually increased with initial and delayed hyperexcitability. Increasing the peak load of the cyclic flexion resulted in larger creep in the passive tissues and required a longer time for recovery of reflex EMG activity and longer delayed hyperexcitability, but development of spasms and hyperexcitability was unaffected. It is conceivable that damage to the viscoelastic tissues elicits an inflammatory process that in turn triggers a transient neuromuscular disorder. The present findings provide a biomechanical and neurophysiological explanation for a common idiopathic low back disorder as well as for the development of a cumulative trauma disorder often seen in workers engaged in repetitive lumbar flexion.