Characteristics of back muscle degeneration in DSK patients
A decrease of muscle size (CSA) and a increase of fatty infiltration (FI) are considered to be two indications of muscle degeneration [
14,
16]. Several studies have evaluated the paraspinal muscle composition and morphology in patients with spinal disorders over the last years; they have suggested that both paraspinal muscles CSA and FI are associated with spinal symptoms, including low back pain, radiculopathy, and spinal stenosis [
17‐
19]. The paravertebral back muscles in patients with degenerative flat back showed significant fat infiltration compared with those in the healthy subjects [
7]. Previous studies used average FI, CSA or RCSA from L1/2 to L5/S1 for comparing the individual muscle degeneration between groups, however, it is still unclear how they change from L1/2 to L5/S1 for individual muscle and whether they are different between muscles at the same spinal level. In the present study, we used the same grey scale range for every muscle at each spinal level, i.e., 0~120, which allows for comparisons between muscles at specific spinal level and between levels for each muscle [
15]. A previous study showed that the FI of multifidus and erector spinae were significantly higher in the degenerative lumbar kyphosis patients than in the healthy volunteers at all levels except L1 [
11]. This may be explained by our study that the FI of multifidus and erector spinae increased from L1/2 to L5/S1. Therefore, the significant higher degree of FI was more prevalent to occur at lower lumbar levels compared to upper lumbar levels. The FI of multifidus and erector spinae were also found to be greater at lower spinal level at symptomatic sway-back patients and patients with low back pain [
15,
17].
RCSA, which reduces the bias due to relative body size of each individual, might reflect the severity of degenerative spinal disorders [
11]. The RCSA of multifidus and psoas increased from L1/2 to L5/S1, whereas the RCSA of erector spinae decreased. The RCSA of erector spinae was higher than multifidus and psoas in upper lumbar spinal levels, whereas, it was the converse in the lower lumbar spinal levels. This indicated that the degeneration of erector spinae is getting worse from L1/2 to L5/S1 relative to multifidus and psoas. The role of erector spinae at lower lumbar spinal level is severely lost. This is consistent with a previous study that the lumbar muscularity of the erector spinae and multifidus were lower in the degenerative lumbar kyphosis patients than in the healthy volunteers at L4 and L5 spinal level [
11].
The FI of multifidus and erector spinae were found to be higher than psoas, but the RCSA of psoas becomes more greater especially at lower spinal levels. From our results, we can see that the degeneration of psoas was the lightest except L1/2. This is supported by the study that the FI of psoas in degenerative lumbar kyphosis patients at every spinal level was not different from that in healthy volunteers [
11]. The FI in psoas was also found less apparent than in the extensor muscles in flat back patients [
7]. The discrepancy in muscle degeneration could be due to:1) The spinal kyphosis overlengthen the extensor muscles which may aggravate the dysfunction and degeneration of extensor muscles but less affect the flexor muscles. 2) There was a apparent effect of lumbar curvature on lever arm lengths for the back extensor muscles, i.e., the lever arm lengths of the erector spinae in lumbar lordosis were significantly longer than in lumbar kyphosis for all spinal levels [
20]. This may lead to a decreased movement of lumbar spine in kyphosis patients which may cause the degeneration of the extensor muscle. 3) The spinal sagittal imbalance may cause the discrepancy in muscle degeneration between extensor and flexor muscles [
7].
Correlation between back muscle degeneration and spinal-pelvic parameters in DSK patients
The muscular system plays an essential role in the maintenance of postural balance and the lumbar muscle is important for lumbar segmental stability [
18,
21,
22]. Therefore, the defects in the paraspinal muscles are thought to aggravate spinal deformity, i.e., affecting the sagittal and/or coronal balance of the spine column. However, only a limited number of reports have used radiographic methods to assess anatomical changes in the paraspinal muscles of patients with spinal sagittal deformities [
7,
11,
15]. Furthermore, until now there were no reports about the influence of individual muscle degeneration at specific spinal level on the sagittal spinal deformity. Therefore, in the present study, we analyzed the correlation between back muscles muscularity (RCSA) and spinal-pelvic parameters in DSK patients. RCSA is considered to be a better indication for evaluating the muscle strength for maintaining the sagittal alignment of the spine [
7,
15,
23]. Therefore, it is believed that RCSA may correlate with the level of functional impairment in the back muscle in DSK patients.
The multifidus muscle is located deeply, attaching to the lumbar vertebrae, and is considered responsible for small movements to stabilize the spine and maintain the lumbar curvature [
24]. We found that the RCSA of multifidus from L2/3 to L4/5 and RCSA of erector spinae at L4/5 were significantly positively correlated in varying degrees with LL, which indicates that mainly the degeneration of multifidus affects the sagittal spine curvature. In Mitsuru et al.’s study, the L5/S1 multifidus CSA is also found to be significantly correlated with sagittal spinal alignment in degenerative spinal scoliosis patients [
10]. Another study showed that the volume of the lumbar extensor muscles in the lower half of the lumbar spine (caudal to the level of the L3/L4 disc) has a positive correlation with the magnitude of the sagittal lumbar curvature over the same region [
25]. The force-generating capacity of a muscle is related to its physical size and larger muscle forces would be required to provide stability in lumbar spines that had larger curvatures [
26,
27]. The reduction of the strength of the spinal muscles is positively correlated with a reduction of the lumbar curvature. In the present study, the higher RCSA at lower lumbar region is accompanied with larger degrees of LL and TK, this can be explained by the compensation between TK and LL in order to keep the stability of the spine. In addition, we found that the RCSA of multifidus at L1/2 was negatively correlated with SVA. The possible reason could be that in the second layer of multifidus, the distal aspect of muscle fibers that originated from the fascicle from L2 insert into the facet capsule and mamillary process of L5, while those from L3 and more caudal levels insert into the iliac crest, sacroiliac joint, and the sacrum [
28]. The muscle strength at L2 is greater than above. Therefore, the multifidus above L2 may mainly maintain the lumbar curvature, but those below L2 may mainly control the rotation of the lumbar spine. Thus, the degeneration of multifidus at this level may aggravate the TLK which may increase SVA and disturb the sagittal balance.
The erector spinae, which is situated more superficially and spans larger sections of the spine, is considered to have a greater role in producing spinal movement [
29]. We found that the RCSA of erector spinae at L3/4 was positively correlated with PI and RCSA at L4/5 was positively correlated with SS in DSK patients. This indicates that mainly the degeneration of erector spinae at lower lumbar levels correlate with the changes of pelvic parameters. Pelvic incidence represents a constitutional anatomic parameter in each individual. An increased pelvic incidence is usually associated with a high sacral slope [
30]. The erector spinae connects to the posterior pelvis and sacrum which to some extent would control the orientation of the sacrum. The orientation of sacrum can definitely affect the measurements of PI and SS. It was reported that the lower erector spinae obliquity is more pronounced at the level of L4 and L5, and in this region the fascicles of the muscle are capable of generating 40–49% of their total resultant force in the posterior direction [
31]. Therefore, the fat infiltration and atrophy of erector spinae at the lower lumbar level would more likely reduce the muscle function which may affect the pelvic parameters.
No significant correlation was found between RCSA of psoas and the spinal-pelvic parameters at any specific spinal level. In Mitsuru et al.’s study, the L5/S1 psoas CSA also has almost no correlation with sagittal spinal alignment in degenerative lumbar scoliosis patients [
10]. The psoas muscle is primarily a hip flexor; however, there is some evidence to suggest that it also acts as a spine stabilizer [
19,
32]. In the present study, very little fatty infiltration was present in the psoas muscle. It was also reported that the RCSA in low back pain patients with Modic changes in the vertebrae body is bigger than the healthy control people indicating that psoas muscle becomes more active regardless of the presence of degenerative changes of the lumbar spine [
23]. Therefore, it could be speculated that in DSK patients, due to 1) the instability and kyphosis of the spine, and 2) DSK patients have more difficulties doing spine extension, the psoas muscle (flexor) may have more movement compared to extensor muscles. However, from the present study, it is still impossible to establish the nature of the causal relationship between spine sagittal deformity and muscle degeneration, i.e., whether the muscle degeneration leads to the DSK or the muscle degeneration is secondary to the DSK.
In addition, spinal and pelvic balance is dependent not only on the paravertebral muscular tension but also on the degeneration and deformity of the spinal column. In the present study, the collapse of the intervertebral disc and the degeneration of the vertebral body also existed, such as Modic changes. The pathology may affect the sagittal balance and have possible additional roles in kyphotic configuration.
Study limitations
There are some limitations in our study which need further discussion and investigation. First, this study may have been limited by the small number of patients. The scarcity of patients who have degenerative kyphosis deformity and who underwent MRI examination of the lumbar spine was the main causative factor. A large population lased multicenter investigation will be more meaningful and help to clarify and determine the associations between individual back muscle degeneration at specific spinal level and the spinal sagittal alignment. Second, a control group of normal healthy subjects which was lacked in our study would help to observe the muscle degeneration in DSK patients. Third, the fat infiltration of muscles could also be affected by the position of apical vertebrae (e.g., at thoracolumbar or lumbar part). However, due to the lack of type III and IV patients, this question needs further study. Fourth, this is a retrospective, cross-sectional study. Therefore, the causal relationship between the back muscle degeneration and degenerative spinal kyphosis is still unclear. Further studies, such as long-term follow-up studies, will be required to clarify these issues.