A new perspective on dysplastic spondylolisthesis: imaging analysis and hypothesis on the pathogenesis
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Published on: September 16, 2022
Kaiyu Liu1,2, Hengrui Chang1, Haoran Li1
1Department of Spine Surgery, Third Hospital of Hebei Medical University, Shijiazhuang, China.
Background:
Dysplastic spondylolisthesis (DS) is a common spine disease in children and adolescents, and its pathogenesis remains unclear. Few previous studies have focused on the cauda equina in patients with DS. This retrospective case-control study evaluated the imaging findings of patients with DS from a novel perspective and attempted to speculate on its underlying etiology.
Methods:
126 young patients (16-24 years) with DS were selected, and the lumbar spinal canal ratio (LSCR) and disc height index (DHI) of nondiseased segments (L1-L5) were measured. The morphology of the cauda equina was observed via magnetic resonance imaging (MRI). We also measured the filum terminale detection rate (FTDR), filum terminale diameter (FTD), and the relative position of the conus medullaris on MRI. The DS group was compared with the control group. The control group consisted of 126 healthy young individuals who were age- and sex-matched to the DS group.
Results:
Compared with that in the control group, the cauda equina in the DS group was more likely to experience excessive posterior displacement (EPD) (P<0.05). DS patients showed a lower FTDR and smaller FTD at the L4-L5 and L5-S1 segments (P<0.05), and exhibited a higher conus medullaris position (P<0.05). The LSCR in L3-L5 segments was significantly greater in the DS group than in the control group (P<0.05). There was no significant difference in the DHI between the two groups at all lumbar segments.
Conclusions:
Compared with healthy young individuals, patients with DS demonstrate thinner filum terminale, a relatively higher position of the conus medullaris, a wider spinal canal, and a higher incidence of cauda equina EPD. Based on these imaging differences, we explored the potential causes of DS and put forward the compensatory spondylolisthesis hypothesis.