Here we conducted a retrospective study to evaluate the lumbar MR images of 209 patients with severe LSS. In total, 290 lumbar sections were diagnosed severe LSS based on our inclusion criteria, and the 248 intervertebral discs that were assigned to the positive Sedsign group. There were only 2 section at the L1/2 level and 12 at the L2/3 level were diagnosed severe LSS, which all were assessed as positive Sedsign(100%). Meanwhile, the incidence of a positive Sedsign increased to 76 in 87 L3/4 levels (87.36%) and 158 in 189 L4/5 levels (83.6%). Therefore, the overall incidence of a positive Sedsign was 85.52% in this study. Our results suggested a positive Sedsign was most common in the lower lumbar spine, which is consistent with the segments that show a high incidence of LSS [15, 16], and further suggested that the positive Sedsign was sensitive to the diagnosis of severe LSS. In addition, our result was also consistent with those reported previously. Tomkins-Lane et al.  reported that the sensitivity of Sedsign scoring was 60–96% in severe LSS. In another study, the Sedsign was positive in 100% of patients with severe LSS . All the above findings all demonstrated that a positive Sedsign should be used as an image parameter for the diagnosis of and screening for LSS in clinical practice.
Although the Sedsign has been reported to be high diagnostic sensitivity, specificity, and efficacy and good clinical application value for the diagnosis of LSS [11–14]. However, the pathogenesis and correlated risk factors of positive Sedsign was still unclear. In this study, the PAD of spinal canal, as a linear indicator of the spinal canal, were measured the distance from the midpoint of the anterior wall to the midpoint of the posterior wall, which was used to assess the degree of spinal stenosis in the sagittal plane. There was no significant difference in the PAD between the positive and negative Sedsign groups in present study, although the ROC curve for the PAD showed a mid-correlation between a positive Sedsign and the PAD. The mainly reason may be the physiologically invalid cavity filled with adipose tissue existed between the posterior of the dural sac and the posterior wall of the spinal canal, which may affected the PAD of spinal canal to reflect the degree of spinal canal stenosis effectively. In addition, the CSA of dural sac, as spinal canal area parameter, was superior to vertebral canal diameter line parameters in diagnosing LSS, due to the characteristics of the spinal canal morphology, some degenerative changes occur in the non-midline part of the spinal canal often induced lateral recess stenosis and finally lead to reduction in spinal canal volume. However, some researcher considered that the CSA could be insufficient as a diagnostic tool [19, 20]. Lohman et al  confirmed that the degree of LSS and the CSA of the dural sac had no significant correlation with the severity of clinical symptoms. Our results also showed that the minimum CSA was not significantly different between the positive Sedsign group and the negative Sedsign group, at the same time, the ROC curve also showed that there was no significant correlation between the prevalence of a positive Sedsign and the minimum CSA. Thus, it is also believed that the CSA of dural sac and PAD of spinal canal can’t fully explain the involvement of nerves in LSS due to the great individual differences.
To further investigate the possible pathogenesis that leads to a positive Sedsign, we conducted a novel radiological parameter, the maximum cross-sectional area difference (CSAD) of the dural sac, to describe the narrowing change of the dural sac. In present study, we observed the sagittal and axial MR images of the patient with severe LSS who was determined to have a positive Sedsign at the L4/5 level(Fig. 5). The dural sac was pushed ventrally or toward the center of the spinal canal by posterior compression in the region where the most severe narrowing occurred (Fig. 5c), and the CSA was at its minimum in this scan image. However, the dural sac at the adjacent sites was less compressed, as shown in Fig. 5b, and the corresponding CSA was more normal. The maximum CSAD of the dural sac was large, which indicated an acute change in the dural sac between the most narrow section and the normal section. As a result, the nerve roots were pulled toward the center of the spinal canal and a positive Sedsign was observed on the MR image. In contrast, when the maximum CSAD was small, there was only minor variation in the dural sac between the level at which narrowing occurred and normal levels, resulting in minimal displacement of the nerve roots and the absence of a positive Sedsign in the MR image at the levels adjacent to the stenosis. Meanwhile, the significant difference also were observed in the maximum CSAD between the positive group and the negative group, and the ROC curve result also showed that there was the highest correlation between the maximum CSAD and incidence rate of positive Sedsign. All these results suggested that the positive Sedsign is more closely related to a change in the dural sac caused by posterior compression at the level of stenosis, which may be the main reason for the appearance of sedimentation syndrome.
To verify the hypothesis, two posterolateral parameters, thickness of ligamentum flavum(TLF) and degeneration of facet joint(DFJ), were further assessed their correlation with the positive Sedsign. The ligamentum flavum and facet joint are the main structures that make up the posterior and lateral spinal canal walls, and has a protective effect on the spinal cord, which had been confirmed to be important roles in the development of LSS [23–25]. TLF and DFJ can induce a decrease in the central tube volume by compression from the behind a dural sac, which is the cause of LSS [26–28]. Therefore, we analyzed the TLF and DFJ between the two groups and found a significant difference for each of these parameters between the positive and negative groups. In addition, The ROC curve result also showed that a positive Sedsign was significantly correlated with the grade of DFJ and the TLF. All these demonstrated that a positive Sedsign was high related to risk factors from the posterior spinal canal. This would also explain why there is a different prevalence of a positive Sedsign between cases of severe LSS and moderate/mild LSS. The change of compressed dural sac was gently in patients with mild-to-moderate LSS, and for whom the MR images rarely show a positive Sedsign. However, when the dural sac(nerve roots or the cauda equina) was obviously squeezed from the posterior side and moved sharply toward the center or ventrally of the spinal canal at the level where stenosis occurred. The adjacent unaffected O nerve roots (or the cauda equina) were also pulled to shift center or ventrally of the spinal canal, a positive Sedsign was observed in MR images. Bartz et al reported that a positive Sedsign was more common when the epidural pressure was increased in LSS patients, which also indirectly supports our results.
Of course, as LSS from complex pathophysiological changes, there are many factors that can decrease the volume of the spinal canal, such as lumbar kyphosis [30, 31], loss of physiological lordosis , giant central lumbar disc herniation [33, 34], and lateral recess stenosis , and can result in typical clinical symptoms of LSS. Not all LSS cases will show a positive Sedsign, which suggests that there are limitations of Sedsign determination in clinical practice. In addition, in the current study, we focused only on the distribution of Sedsign in patients with severe LSS. The validity of this theory on a wider scale is not currently known. Further study is needed to determine the distribution of a positive Sedsign among patients with mild-to-moderate LSS.