BACKGROUND CONTEXT: Spinal burst fractures are a significant cause of spinal instability and neurologic impairment. Although evidence suggests that the neurologic trauma arises during the dynamic phase of fracture, the biomechanics underpinning the phenomenon has yet to be fully explained. Interpedicular widening (IPW) is a distinctive feature of the fracture but, despite the association with the occurrence of neurologic deficit, little is known about its biomechanics. PURPOSE: To provide a comprehensive in vitro study on spinal burst fracture, with special attention on the dynamics of IPW. STUDY DESIGN: Experimental measurements in combination with computed tomography scanning were used to quantitatively investigate the biomechanics of burst fracture in a cadaveric model. METHODS: Twelve human three-adjacent-vertebra segments were tested to induce burst fracture. Impact was delivered through a drop-weight tower, whereas IPW was continuously recorded by two displacement transducers. Computed tomography scanning aided quantifying canal occlusion (CO) and evaluating sample anatomy and fracture appearance. Two levels of energy were delivered to two groups: high energy (HE) and low energy (LE). RESULTS: No difference was found between HE and LE in terms of the residual IPW (ie, post-fracture), maximum IPW, or CO (median 20.2%). Whereas IPW was not found to be correlated with CO, a moderate correlation was found between the maximum and the residual IPW. At the fracture onset, IPW reached a maximum median value of 15.8% in approximately 20 to 25 milliseconds. After the transient phase, the pedicles were recoiled to a median residual IPW of 4.9%. CONCLUSIONS: Our study provides for the first time insight on how IPW actually evolves during the fracture onset. In addition, our results may help shedding more light on the mechanical initiation of the fracture.
CORE (COnnecting REpositories)
CORE (COnnecting REpositories)