In recent years many reports about the relationship between the neurologic damage and the spinal canal compromise in burst fracture have been published. But the mechanism and relationship between neural compression and recovery are poorly
understood.
To investigate the relationship between the traumatic canal impingement and the neurologic improvement and to find the factors affecting the improvement of the neurologic symptoms, the authors evaluated the one hundred and forty-eight consecutive
cases
who had been treated under the diagnosis of burst fracture on the thoracolumbar spine from Jan. 1986 to Dec. 1993 in Severance Hospital.
The spinal canal was measured on the CT scan using microcomputer assisted image analyzer and Frankel grade was used to evaluate the neurologic status of the patients.
@ES The results were as follows:
@EN 1. Ninety-one patients were injured in a fall down from a height, forty two patients suffered from injuries related to a motor vehicle accident, and fifteen were injured by other causes. The most common site of injury was Ll which accounted
for
32.4% of all of the injuries.
2. Of the one hundred and forty-eight patients studied, twenty-three had Frankel A lesion and seventy-seven had no deficits on initial examination. Forty-eight patients had incomplete lesions and twenty-nine patients had neurological
improvements
at
last follow-up.
3. of the one hundred and six patients who had surgical treatment, ninety-eight had posterior decompression with posterolateral spinal fusion, five had anterior decompression with anterior interbody fusion, and three had anterior decompression
with
posterior fusion.
4. In the groups without neurologic deficits, the mean neural canal impingement was 35% and 52% in the groups with neurologic deficits at the first examination.
5. The amount of canal impingement was reduced from fifty-four percent to thirty-one percent in the neurologically unimproved group and from fifty-three percent to thirty three percent in the neurologically improved group.
6. Fifty three(63%) of the eighty-fort patients with disruption of canal had neurologic deficits, while twenty two(34%) of the sixty-four patients without disruption of canal had neurologic deficits.
7. Thirty-one (58.5%) of the neurologically damaged fifty-three patients with disruption of the posterior element improved neurologically at last follow-up, but only six(27.3%) of twenty-two patients without * disruption of the posterior element
had
neurologic improvement.
In conclusion, at each level of the spinal cord the difference in the canal impingement between the cases with neurologic deficits and the cases without neurologic deficits was statistically significant. So higher percentage of canal impingement
caused
more neurologic injury. The disruption of posterior element indicated a more significant neurologically injured status at the first examination but the presence of posterior element disruption meant a high possibility of neurologic recovery.
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