The effect of post-injury spinal position on canal occlusion in a cervical spine burst fracture model.
METHODS
The canal space of burst-fractured, human cervical spine specimens was monitored to determine the extent to which spinal position affected post-injury occlusion.


OBJECTIVE
To test the null hypothesis that there is no difference in spinal canal occlusion as a function of spinal positioning for a burst-fractured cervical spine model.


BACKGROUND
Although previous studies have documented the effect of spinal positioning on canal geometry in intact cadaver spines, to the authors' knowledge, none has examined this relationship specifically in a burst fracture model.


METHODS
Eight human cervical spine specimens (levels C1 to T3) were fractured by axial impact, and the resulting burst injuries were documented using post-injury radiographs and computed tomography scans. Canal occlusion was measured using a custom transducer in which water was circulated through a section of flexible tygon tubing that was passed through the spinal canal. Any impingement on the tubing produced a rise in fluid pressure that was monitored with a pressure transducer. Each spine was positioned in flexion, extension, lateral (and off-axis) bending, axial rotation, traction, and compression, while canal occlusion and angular position were monitored. Occlusion values for each position were compared with measurements taken with the spine in neutral position.


RESULTS
Compared with neutral position, compression, extension, and extension combined with lateral bending significantly increased canal occlusion, whereas flexion decreased the extent of occlusion. In extension, the observed mechanism of occlusion was ligamentum flavum bulge caused by ligament laxity resulting from reduced vertebral body height.


CONCLUSIONS
Increased compression of the spinal cord after injury may lead to more extensive neurologic loss. This study demonstrated that placing a burst-fractured cervical spine into either extension or compression significantly increased canal occlusion as compared with occlusion in a neutral position.
Ching
R P
RP
Harborview Biomechanics Laboratory, Department of Orthopaedics, University of Washington, Seattle, USA.
Watson
N A
NA
Carter
J W
JW
Tencer
A F
AF
D001696:Biomechanical Phenomena; D002574:Cervical Vertebrae / Q000000981:diagnostic imaging / Q000293:injuries* / Q000503:physiopathology; D006801:Humans; D017843:Ligamentum Flavum / Q000473:pathology; D013115:Spinal Canal / Q000293:injuries*; D013117:Spinal Cord Compression / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D016103:Spinal Fractures / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology; D014057:Tomography, X-Ray Computed