There are numerous causes of LBP, so it is difficult to clearly identify the exact cause . Ko et al.  reported that they are related to the cross sectional area (CSA) and the sedimentation sign (SedSign) but have little to do with SedSign and LLRP, LBP, and NIC, and they insisted that the spinal area has nothing to do with lower leg pain and LBP except for severe spinal stenosis. However, according to many authors, the narrower CSA is in CLSS, the more pressure is applied to the nerve root in the cauda equina . It is known that such central compression of the cauda equina is extensively involved in LBP as well as LLRP and NIC [19–21]. This is in line with the fact that there is severe LBP among the “red flag” symptoms of the cauda equina syndrome due to the severe cauda equina compression . According to Ogikubo et al. , the extent of lower leg pain is more severe than that of LBP mainly in LSS, and because lower leg pain can deteriorate by actions such as ambulation and changes in posture, the symptoms in the lower legs are emphasized. In addition, they reported that the narrower the CSA is in the spinal canal, the shorter the walking distance is with severe lower leg and LBP, which led to the poor quality of life. Although LBP can be caused by degenerative intervertebral joints apart from the direct cauda equina compression, Ogikubo et al.  claimed that improvements in LBP as well as LLRP are considered feasible if the CSA within the spinal canal is extended.
Jones et al.  presented that decompression surgery for LSS is effective in improving LBP up to 6 weeks after surgery in patients with central and lateral recess spinal stenosis and in some patients even with spondylolisthesis and scoliosis. But as studies on pain and functional outcomes were conducted 6 weeks and a year after surgery, the changes between the periods were not available and the methods of surgery are almost half-mixed with a laminectomy, in which the spinous process and nearly total laminal are removed, and a laminotomy, which is the partial removal of the lamina. In addition, it is doubtful whether patients with LBP can recover in up to 6 weeks due to pain by muscle damage in surgery; however, the conclusion is that there was statistically significant improvement 6 weeks and a year after surgery, and the outcomes were similar to those of the authors in that they were more than MCID at 6 weeks and less than MCID at a year after surgery.
However, back muscle injuries in surgery can affect LBP after surgery. Decompression through the standard open posterior approach that we conducted is the most commonly used decompression technique; however, there is much manipulation of paraspinal muscles, and iatrogenic muscle damage is caused due to detachment and retraction of muscles. There is a study in which as for one-level lumbar decompression, there is no relationship between LBP and muscle damage , and some authors [10, 15] reported that LBP continues up to 4 years after surgery and shows improvement after that. Several researchers claim that over time after surgery, degeneration and denervation of damaged back muscles, particularly multifidus muscles after surgery progress, can cause atrophy and fatty degeneration of muscles and at last can be a cause of LBP [26–29]. It was observed in this study that one-level lumbar decompression surgery reduces LBP in patients up to 6 months after surgery, whereas it slowly deteriorates for 6 months afterward.
There are several limitations in this study. First, the follow-up period of 1 year is somewhat too short, but as the period increases, LBP can be affected by various causes such as degeneration of paraspinal muscles and facet joints and degeneration of the intervertebral discs besides decompression surgery itself of LSS. In this regard, the period was limited to a year. Second, no evaluation was made on what causes LBP apart from decompression of LSS. Specifically, the analysis was insufficient with respect to the relationship between stenosis of the CSA within spinal canal in the radiographic imaging before surgery and symptoms of patients, and between decompression of the CSA after surgery and symptoms of patients. Therefore, obtaining and analyzing the additional imaging data after surgery will be required. Third, the sample size was too small with 39 cases and as this is a retrospective study without a control group which is the weakness of this research, it is considered that an extensive and prospective research will be required afterward.