To our knowledge, this study is the first to evaluate the characteristics and location of LBP in patients with LDH treated with discectomy. According to the previous study analyzed detailed and bilateral VAS scores for LSS patients, LBP in patients with LSS before surgery was significantly greater while standing, but pain was reduced by decompression surgery, with LBP improving equally on the affected and opposite sides [6]. In our study, LBP during motion was significantly greater in patients with LDH before surgery, and the LBP in motion on the affected side was reduced by discectomy. This pattern of LBP relief suggests that radicular LBP is improved by nerve root decompression surgery, as mentioned in previous reports [1, 6]. Despite this similarity regarding nerve root decompression, however, greater LBP during motion that occurred with LDH patients was different than the increased LBP while standing found in LSS patients. For this reason, we speculate that nerve root compression in patients with LDH usually occurs with a more acute onset compared to LSS. In addition, this difference in LBP characteristics may be influenced by the degree of disc and endplate degeneration in LDH patients compared to LSS patients because LDH patients tend to be younger than LSS patients.
Another noteworthy point gleaned from our findings was that residual LBP was most pronounced while sitting. A recent report has indicated that higher intradiscal pressure while sitting may result in LBP in the presence of lumbar degenerative disc diseases [11]. It was reported that pathological mechanisms of discogenic low back pain included sensory nerve ingrowth into the disc, upregulation of neurotrophic factors like nerve growth factor and inflammatory cytokines, and mechanical stress [12, 13]. Our findings of residual LBP while sitting and changes in Pfirrmann grade, when taken in combination, leads us to conclude that it is likely the load and pressure on the disc were causal in residual LBP while sitting. Alternatively, it is also well known that Modic changes influence LBP [14]. Ohtori et al. reported favorable surgical outcomes for LDH complicated with Modic type I [15]. Although LEP improvement was obtained in patients with Modic change in our study, the residual LBP in MC group leads us to believe that changes in load and inflammation at the endplate may also be causal in residual LBP while sitting.
Recent reports indicated that performing a minimally invasive discectomy using a tubular retractor under a microscope or endoscope are feasible in the treatment of LDH [16, 17]. Including conventional discectomy, in our study we compared these 3 surgical procedures. Residual LBP at 3 months after surgery was greater in group T because the baseline of LBP before surgery was significantly greater in this group. However, the residual LBP at 1 year follow up was equal with all 3 surgical procedures. This, along with previous reports, suggests that surgical invasion of the paraspinal muscles does not influence residual LBP [6, 16]. While no reports were found describing the relationship between surgical levels and residual LBP, in our study, residual LBP was significantly greater in patients with herniations at L3/4. It is hard to explain this phenomenon. However, we speculate that this may have been the case because patients with L3/4 herniations were highly complicated and also had L4/5 or L5/S disc degenerations. Further investigation with a larger sample size is needed to understand this phenomenon.
The present study has several limitations. First, this study is observational, and we did not evaluate detailed and bilateral LBP VAS scores of patients who solely underwent conservative treatment. In our study some of the patients underwent conservative treatment at another hospital, and they wished to undergo surgical treatment as soon as possible, leaving them no time to evaluate further conservative treatment. Further prospective investigation will be needed. Second, the present study excluded patients complicated with dynamic instability or patients with lateral herniations who underwent fusion surgery because we wanted to avoid LBP caused by instability of discs and facet joints [18]. Furthermore, the present study also excluded cases which, unfortunately, had a recurrence of herniation in the short term (less than a year) because we wanted to evaluate residual LBP in the absence of herniation recurrence. If those cases had been included, the results would have been confounded by the fact that they had severe VAS scores under all 3 postural conditions. Third, the present study did not evaluate sagittal alignment. Sagittal imbalance such as pelvic incidence and lumbar lordosis mismatch may contribute to postoperative LBP [19]. Using detailed VAS scores, Aoki et al. indicated that sagittal imbalance after a short segment fusion surgery resulted in residual LBP while standing [20]. Considering our finding that residual LBP while sitting was present at 1 year after discectomy, we speculate that residual LBP is less affected by sagittal alignment. Finally, the follow up after discectomy was incomplete. When patients undergo discectomy and have significant pain relief, they sometimes drop out of care at the outpatient clinic. 18 of 114 (15.7%) cases in our study dropped out. Generally, two years of follow-up is recommended for this type of study. However, in this study, we were compelled to set the follow-up period to 1 year because of a decreasing follow-up rate. Further investigation, like a prospective cohort study that follows all the cases fully will be needed to resolve this follow-up rate problem.