Since Sed-sign was first introduced by Barz et al6, an important research focus has been on the evaluation of clinical and radiological characteristics to better distinguish LSS from lower back pain patients. Due to the relatively lower sensitivity in detecting clinically defined LSS in orthopedic clinical cohorts, the Sed-sign does not allow for definitive differential diagnosis of LSS11,12. Compared with non-surgically treated positive Sed-sign patients, favorable outcomes have been reported for patients who underwent surgical treatment9,13. Therefore, Sed-sign seemed to be an indication to help determine the appropriate treatment. Previous studies investigating the Sed-sign have concentrated on the diagnosis of LSS as well as its influence on the surgical outcomes. Evaluation of the reversibility of the Sed-sign after decompression surgery as well as the influence of irreversibility on surgical outcomes is still mandatory.
The current study retrospectively reviewed 82 patients with LSS who underwent surgical decompression at our spine center. The incidence of positive Sed-sign in the current study was similar to that reported in the literature6–8. The definitive disease mechanism for positive Sed-sign remains unknown. The increased epidural pressure at the level of spinal stenosis has been reported as the main cause for positive Sed-sign in patients with LSS14. Barz et al.14 noted that increased epidural pressure at the level of the stenosis may result in tethering of nerve roots in the spinal canal at that level as if held by a mechanical clamp. In the current study, 80.4% of patients showed reversibility of the Sed-sign after decompression surgery performed at the level of stenosis. This tendency was similar to the study performed by Barz et al.10, who reported that 27 of 30 patients had negative Sed-sign after decompression surgery. Together, these results suggested that decompression surgery resulted in reversibility of Sed-sign in most patients. However, it should be noted that not all LSS patients with positive Sed-sign showed reversibility after decompression surgery (Fig. 1). The frequency of patients with positive Sed-sign after decompression surgery in the current study was slightly higher than the study of Barz et al.10 This difference may be due to the fact that only patients who underwent single-level decompression surgery were enrolled in the current study.
Barz et al.9 reported that a positive Sed-sign was associated with limited clinical improvement in non-surgically treated patients. Among patients treated with decompression surgery, those with positive Sed-sign achieved similar clinical improvements when compared with negative Sed-sign patients9. HRQOL in the current study, based on the ODI, VAS, and ZCQ scores, suggested that both R and Ir groups achieved improvements after surgery compared with the preoperative evaluations. This finding was consistent with those of Barz et al.10, who reported that patients with the irreversibility of Sed-sign made improvements in clinical outcomes for ODI, VAS, and ZCQ scores. In the current study, a further comparison between patients with positive and negative Sed-sign after decompression surgery showed that the ODI, VAS, and ZCQ scores in the Ir group were significantly lower than those in the R group. Our findings suggested that the irreversibility of Sed-sign after decompression surgery was associated with poorer clinical outcomes when compared with those with negative Sed-sign at post-operation.
The main mechanisms underlying the irreversibility of positive Sed-sign remain unknown. Possible reasons for positive Sed-sign included insufficient decompression, postoperative hematoma, excessive postoperative scar tissue, and epidural lipomatosis10. Barz et al.10 noted that the reasons for 3 patients with irreversibility of Sed-sign were potentially associated with postoperative complications, including two cases with epidural fat and one case with an epidural cyst. In fact, such complications may also be attributed to abnormal epidural pressure, like insufficient decompression of the LSS. In the current study, similar complication rates were found between those with reversibility and irreversibility of Sed-sign. Based on the multiple logistic regression, our results showed that the primary risk factor for the irreversibility of positive Sed-sign was a postoperative CSA of less than 131.4 mm2. The association between smaller CSA and the irreversibility of Sed-sign may also attribute to the increased epidural pressure, which may be induced by the relatively smaller CSA. Therefore, our results further demonstrated the relationship between increased epidural pressure and formation of positive Sed-sign.
The clinical relevance of this study relates to decreasing the incidence of the irreversibility of Sed-sign and improving HRQOL after decompression surgery. First, decompression at the stenosis level should be performed. Second, postoperative complications, such as epidural fat and hematoma, may also increase abnormal epidural pressure and further influence the reversibility of preoperative Sed-sign. Therefore, complications should be identified and managed as soon as possible.
There were also some limitations in the current study. First, the sample size in the current study was relatively small. Patients enrolled in the current study only underwent single-level TLIF decompression for consistency. The relationship between multi-level decompression and reversibility of positive Sed-sign remains unclear. Second, HRQOL may be influenced by several sagittal parameters. However, further evaluation of sagittal alignments, such as pelvic incidence-lumbar lordosis, was limited due to the retrospective character of the current study. Third, even all of these surgeries were performed by same surgical team and the goal of surgery is to achieve adequate decompression, the effect of insufficient decompression on HRQOL should not be neglected. Therefore, a larger sample size with a detailed evaluation of sagittal alignment should be performed in future studies.