PURPOSE: To assess whether canal compromise determines neurological deficit in thoracolumbar and lumbar burst fractures. METHODS: 105 patients aged 17 to 60 (mean, 34) years who had burst fractures in the thoracolumbar (n=82) and lumbar (n=23) regions were included. Fractures were classified according to the Denis classification. The extent of spinal canal compromise was assessed by computed tomography, and the neurological status according to the modified Frankel grading for traumatic paraplegia. RESULTS: 19 (18%) of the patients had no neurological deficit. Of the remaining 86 (82%) with a deficit, 26 had complete paraplegia. The correlation between the type of the burst fracture and the severity of neurological deficit was not significant (Chi squared=10.57, p=0.835). The mean extent of spinal canal compromise in patients with deficits was 50%, whereas in patients with no deficit it was 36%. The difference between the extent of canal compromise and the severity of neurological deficit at the thoracolumbar and lumbar spine was not significant (p=0.08). Further subanalysis revealed a significant correlation at T11 and T12 (p=0.007) but not at the L1 (p=0.42) level. CONCLUSION: When studying neurological deficit, T11 and T12 injuries should be analysed separately from L1 injuries.
PURPOSE: To assess whether canal compromise determines neurological deficit in thoracolumbar and lumbar burst fractures. METHODS: 105 patients aged 17 to 60 (mean, 34) years who had burst fractures in the thoracolumbar (n=82) and lumbar (n=23) regions were included. Fractures were classified according to the Denis classification. The extent of spinal canal compromise was assessed by computed tomography, and the neurological status according to the modified Frankel grading for traumatic paraplegia. RESULTS: 19 (18%) of the patients had no neurological deficit. Of the remaining 86 (82%) with a deficit, 26 had complete paraplegia. The correlation between the type of the burst fracture and the severity of neurological deficit was not significant (Chi squared=10.57, p=0.835). The mean extent of spinal canal compromise in patients with deficits was 50%, whereas in patients with no deficit it was 36%. The difference between the extent of canal compromise and the severity of neurological deficit at the thoracolumbar and lumbar spine was not significant (p=0.08). Further subanalysis revealed a significant correlation at T11 and T12 (p=0.007) but not at the L1 (p=0.42) level. CONCLUSION: When studying neurological deficit, T11 and T12 injuries should be analysed separately from L1 injuries.