Experimental models of intervertebral disc and facet joint degeneration were created in vivo in the porcine lumbar spine for studying spinal kinematics, using a dynamic technique.
To quantify the changes in spinal kinematics and the stabilizing capacity of the lumbar musculature caused by chronic lesions in the intervertebral disc and facet joints.
Segmental kinematics are detrimentally altered by acute injury to passive structures of the motion segment. However, stimulation of the surrounding musculature adds stability to the motion segment. The in vivo kinematics of a degenerated lumbar motion segment and the stabilizing function of the surrounding musculature have not been quantified dynamically.
Forty-four pigs were used in six chronic lesion models: sham, disc anulus, disc nucleus, facet capsule, facet joint slit, and facet joint wedge. Three months after injury, an instrumented linkage was used to measure continuously the sagittal kinematics of the L3-L4 motion segment during flexion-extension, with and without stimulation of the lumbar paraspinal musculature. Flexion-extension end point and maximum ranges of motion, and hysteresis were analyzed.
Significant alterations in the kinematics caused by chronic lesions were observed, particularly when using the maximum range of motion and when comparing changes in axial translation. Muscular stimulation reduced the hysteresis in the sham, facet capsule, and disc nucleus groups; however, increased hysteresis was observed in the remaining lesion groups.
The kinematic behavior of motion segments with chronic lesions was established. The maximum range of motion, which must be measured using a dynamic technique, was a more sensitive parameter for identifying changes in segmental kinematics caused by chronic lesions than was the end range of motion. The lumbar musculature was less efficient overall in stabilizing the motion segment, possibly because of altered mechanisms in the neuromuscular feedback system.
From the Department of Orthopaedics, Sahlgrenska University Hospital, Göteborg, Sweden.
Financial support was provided by the the Swedish Council on Work Life Research, Stockholm, Sweden, and the Greta and Einar Askers Fund, Göteborg, Sweden.
Acknowledgment date: July 7, 1997.
Acceptance date: July 7, 1997.
Device status category: 1.
Address reprint requests to: Allison M. Kaigle; Department of Orthopaedics; Sahlgrenska University Hospital; Guldhedsgatan 19, S-413 45; Göteborg, Sweden.