Abstract

Based on the "uncoupled neuro-osseous growth" theory, the hypothesized etiology of adolescent idiopathic scoliosis (AIS), a shorter spinal cord or a higher conus location, could be found in AIS patients. However, there are no case-control studies with large samples regarding the conus position in AIS patients. This study is performed to determine the positions of the conus medullaris in AIS patients with a large curve magnitude when compared with healthy adolescents and to investigate the relationships of the conus locations with patients' age, sex, curve magnitude, and curve pattern. Two hundred forty AIS patients with a Cobb angle greater than 40 degree were included in this study, and 120 age-matched healthy adolescents were recruited to serve as controls. Both AIS patients and healthy controls displayed normal on neurological examinations. On sagittal magnetic resonance images of the spine in both groups, the position on the conus medullaris relative to lumbar vertebrae and intervertebral disk space was measured according to a standard method. There was no significant difference in the distributions of the positions of the conus medullaris in AIS patients and healthy controls (P = 0.448). In both groups, the mean position of the conus medullaris was located at the same level, which was the lower 1/3 of L1 (range: the middle third of T12 to L2-3 disk space). The conus positions were neither significantly different among adolescents of different ages (P = 0.662 in AIS and P = 0.897 in controls) nor between boys and girls (P = 0.875 in AIS and P = 0.675 in controls). It was shown that the conus position was not significantly different among AIS patients with different curve severity (F = 0.314, P = 0.731) and curve patterns (F = 0.097, P = 0.756). The mean and the distribution of the conus locations were similar for AIS patients and the controls. No significant associations of the conus position with curve severity and with curve patterns were found, indicating that the conus location might not be involved in the pathogenesis and curve progression of AIS. Level III.

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