Canal and intervertebral foramen encroachments of a burst fracture: effects from the center of rotation.

Abstract

The neural spaces of thoracolumbar burst fractures were investigated in an in vitro biomechanical study. To evaluate encroachments of spinal canal diameter and intervertebral foramen area as functions of where the center of rotation is located during flexion and extension. Decompression of the neural spaces is important for the recovery of neural function in a patient with a burst fracture injury. A few biomechanical studies have documented the decompression of the neural elements by adjustment of posterior fixation devices. However, the device adjustments have been device specific and ill defined. No study has investigated the neural decompression phenomenon with precisely defined multiple adjustments. Burst fractures were produced at L1 vertebra in nine T11-L3 human spinal segments. Specimens were flexed and extended around five different centers of rotation located in the mid-L1 plane. The spinal canal diameter and intervertebral foramen area encroachments were quantified in maximum flexion and extension around each center of rotation using lateral radiographs. The average canal encroachment of 42.6% changed in flexion (32.2-48.5%) and extension (36.3-44.2%) by location of the center of rotation. The average intervertebral foramen area encroachment was decreased to a greater extent more often in flexion than in extension because of where the center of rotation was located. Both flexion and extension can decompress canal and foramina, depending on the choice for the location of the center of rotation. If lordotic posture is preferred clinically, then the optimal choice may be extension around the center of rotation located at the tip of the spinous process of the burst vertebra.