Introduction
Lumbar spinal stenosis (LSS) is a common degenerative spinal disease in the older population. After a detailed report on transforaminal lumbar interbody fusion (TLIF) surgery by Harms et al. [
1] in 1998, TLIF became the major surgical treatment for LSS. Cole and McCall [
1] reported that TLIF is minimally invasive, has less structural exposure, and minimises lamina, facet, and pars dissection compared with posterior lumbar interbody fusion (PLIF). Adjacent segment degeneration (ASD) is a major concern after fusion surgery. However, few studies have discussed ASD of the lumbar foramen [
2‐
5].
The pathology of lumbar foraminal stenosis was first reported in 1927 [
6]. Lumbar foraminal stenosis might have been caused by posterolateral osteophytes, herniated discs, laterally bulging annulus fibrosus, subluxation of the facet, and hypertrophic ligamentum [
7]. The concept of foraminal stenosis was defined as lateral spinal stenosis [
6]. Notably, the reconstructed sagittal images provide better visualisation of the foramen. The L5-S1 foramen, because of its anatomical and functional features and lumbosacral junction, is more susceptible to significant loading from the trunk and tends to have a higher incidence of degeneration [
7].
The lumbar paraspinal muscle plays a vital role in the stability of the entire spine and the effectiveness of spine surgery. Muscle quality can be evaluated using the total cross-sectional area (tCSA) and fatty infiltration (FI). The previous studies have reported that patients with a lower CSA and higher muscle FI are more likely to have low back pain (LBP), ASD, facet joint arthropathy, and spinal misalignment [
8‐
13].
To our knowledge, the correlation between paraspinal muscle quality and adjacent segment lumbar foraminal stenosis degeneration (ASLFSD) has not been previously investigated. Consequently, this study aimed to investigate the effects of preoperative paraspinal muscle tCSA and FI on L5-S1 ASLFSD after L4–L5 TLIF.
Discussion
ASD is common after lumbar fusion surgery, and adjacent foramen segment stenosis is often observed. Ryu et al. [
18] reported that reoperation is most likely associated with foraminal stenosis in patients with ASD (
p = 0.001). Our study aimed to investigate the relevance of preoperative paraspinal muscle quality in the occurrence of L5-S1 ASLFSD after L4–5 TLIF.
Changes in PDH, D–F, and FH could potentially lead to a reduction in FA owing to the anatomical structure of the intervertebral foramen. In our study, FH and FA were significantly reduced at 1 year postoperatively compared to preoperative foraminal measurements, and PDH, D–F, FH, and FA were all significantly reduced at the final postoperative follow-up compared to 1 year postoperatively. Although our study follow-up period was short, foraminal stenosis did occur after surgery. The reasons for the occurrence of L5-S1 ASLFSD after L4–5 TLIF also varied. The previous studies have shown that fusion surgery increases pressure in the intervertebral disc and facet joint in adjacent segments [
1,
19‐
23]. The increase in biomechanical pressure promotes disc degeneration, further disc herniation, extrusion of the lumbar foramen, and a decrease in foraminal height [
20,
24‐
26]. The accelerated degeneration of facet joints after fusion surgery may be another contributing factor to the change in foramen morphology [
9‐
12].
Moreover, correlations between foraminal parameter changes, paraspinal muscle tCSA, and FI were analysed. Regardless of whether it was 1 year or the final postoperative follow-up, the FI of the paraspinal muscles was negatively correlated with changes in the foraminal measurements, though there was no significant correlation with PDH. Our results indicate that the tCSA of the paraspinal muscle is not a decisive factor affecting the degeneration of the intervertebral foramen and that the degree of muscular FI is a risk factor for the occurrence of ASLFSD. To further validate our hypothesis, we compared the difference in paraspinal muscle quality between patients with severe spinal stenosis (grade 3, based on the CT classification system of LFS) and general patients (grades 0, 1, and 2, based on the CT classification system of LFS) during the final follow-up. The patients of the grade 3 have higher degree of paraspinal muscle FI. However, we also found that tCSA of the paraspinal muscle was larger in these patients. These increases in tCSA have not brought improvement to the patients. So, we believe that muscular FI is the more valuable for predicting L5-S1 ASLFSD after L4–5 TLIF. Then, how do the paraspinal muscles work?
Paraspinal muscle quality influences surgical efficacy. The previous studies have reported that a smaller tCSA is associated with a poorer fusion rate in patients undergoing PLIF [
27,
28]. Wang et al. [
29] demonstrated that a smaller multifidus tCSA and higher multifidus FI on preoperative MRI scans were significantly associated with higher ODI scores both preoperatively and postoperatively. In the lumbar muscle system, the psoas attached directly to the vertebral bodies anterolaterally acts as the primary flexor muscle group, whereas the multifidus and erector spinae act as strong extensor muscle groups [
19]. Additionally, McGill et al. [
30] showed that the erector spinae reduce the compression force from 20 to 35% in a body experiment under external compression. When the multifidus was studied as an individual muscle, it acted more as a segmental stabiliser to enable the separate control of individual vertebrae [
31]. Electromyography studies have confirmed this result and revealed that the multifidus plays a role in controlling intersegmental motion [
32,
33]. Thus, we strongly believe that, with a higher paraspinal muscle, the FI was more likely to develop ASLFSD after fusion surgery.
Why did we choose the L5-S1 level as our research subject? Regarding anatomical factors, the L5-S1 disc is at the lowermost part of the spine and is the most variable area of lumbar spine activity. The disc of L5-S1 is also more prone to degeneration in lumbar fusion and LBP patients [
34,
35]. However, the presence of preoperative disc degeneration did not show a significant correlation with the development of postoperative ASD [
36]. A study on the degenerative stenosis of the L3–4 intervertebral foramen after L4–5 TLIF surgery can be further investigated.
This study has some limitations, including a relatively small sample size and short follow-up period. Furthermore, this study did not include the intervertebral foramen of L3–4. Undoubtedly, with longer follow-up times, the incidence of ASLFSD following TLIF surgery will increase, and with a larger sample size, the association between ASLFSD and paraspinal muscle quality will become more apparent. Therefore, a long-term and large-scale study can be extended in future. Additionally, since we only considered preoperative MRI appearance of the paraspinal muscles, postoperative muscle atrophy and fatty infiltration of the patients were not further discussed. Finally, spinal sagittal balance is another influencing factor that cannot be ignored, we will further verify its relationship with ASLFSD in our subsequent research.
Nevertheless, this study has several strengths. All surgical operations were performed in the natural cleavage plane between the multifidus and longissimus muscles to minimise the damage to the muscle [
37]. This approach also has the advantages of less blood loss, fewer ASD rates, less damage to paraspinal muscle, and fewer additional surgical procedures [
38,
39]. Moreover, our measurements of the foramen area were comprehensive, including foraminal height and width, which could help us understand ASLFSD in a three-dimensional way. Additionally, this study was the first to evaluate spinal muscle quality as a prognosticator of ASLFSD after TLIF surgery; thus, this study could be a cornerstone for further studies analysing the factors influencing postoperative radiological foraminal stenosis in fusion surgery.
In the previous studies, research on ASLFSD after lumbar fusion surgery was scarce. Our research can make that clinical physicians have a deeper understanding of ASLFSD and pay more attention to this issue, and provide some theoretical basis for future research.
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.