The maintenance of spinal sequence and sagittal balance have been fully realized close to paraspinal muscle groups, especially multifidus and erector spinae [6, 7, 13]. Yagi et al. [7] conducted a multicenter retrospective study with 60 ASD patients and found that CSA of multifidus and erector spina was less, significantly correlated with the sagittal spinal disorders. They found that the spine sequence and the paravertebral muscles are interacting. In fact, there was a interaction between paravertebral muscles and spinal sequence, especially in the elderly [13, 14]. In addition, Mannion et al. [15] found that the degeneration of paravertebral muscle is a secondary progress related to the severity of scoliosis in ASD by histochemical analysis.
For ASD patients, Banno et al [7] found that the malformation of sagittal parameters and lumbar spine were correlated with CSA of multifidus even if the weight and age were adjusted. While the muscle content in patients with thoracolumbar deformity was seldom focused on. The higher incidence and exposure rate in- and out-patient of DTLK with LSS in middle to old group forced it essential to indentify the relationship between TLK and paravertebral muscles [16]. However, usual methods for measuring paravertebral muscles were complicated and time-consuming, so many outpatient cases could not be measured in time. The concept of LCIV, innovated by Takayama et al., made the measurement easy and efficient, wide in use and with shorter learning-curve [12]. There were not many studies on body shape and sagittal deformity. Some reports showed obesity was a risk factor in promoting the occurrence of degenerative scoliosis while others believed that the absolute muscle composition related to sagittal sequence instead of obesity presented by FI [1, 17]. Our study found the muscle content with larger BMI was more than cases with lower BMI while the body shape was irrelevant to TLK in control group. Similarly, the degree of TLK in DTLK group did not correlated to BMI but to the content of paraspinal muscle.
Takayama et al. [12] found LCIV and CSA were highly correlated in all lumbar segments (r = 0.708–0.789) and LIV was negatively correlated with age, but there was no statistical difference among people over 50 years old. Our data showed that LCIV in DTLK group was less compared to normal ones. On the one hand, local kyphosis of the thoracolumbar and upper lumbar spine with DTLK approximated spinous processes to the skin in this range, even protruding over the surface. On the other hand, the posterior muscle groups got thinner under pressure with abnormal distribution by kyphotic bone structure, supporting the point that CSA of paraspinal muscle was in correlation to progressive kyphosis [9, 18]. Therefore, the intergroup difference on LCIV mainly concentrated on the upper lumbar spine and the lower region was almost comparable. The LCIV gradually increased from cranial to caudal vertebrae regardless of the DTLK or the control group, which mainly due to the sagittal lordosis in lumbar spine sine the anatomical structure enlargered the interval from spinous process to the apex of both muscle skin surface. In addition, the iliac crest and sacrum provided the attachment point of sacrospinous muscle and further thichened the paravertebral muscles in this area [12].
As the initial spinal-pelvic parameter, the loss or increase of LL will cause adjustment of pelvis rotation and proximal thoracolumbar kyphosis for compensating [19, 20]. In this study, the ratio of patients with increased and decreased LL were 20.6% and 28.6%, respectively. For those with larger LL, there is deepened skingrooves and higher apex of posterior muscles. While for lower LL ones, although surrouded by psoas and erector spinae, the content of paraspinal muscle decreased with spine kyphosis and less space for muscle attachment, together with the muscle strength of the lower back muscles significantly frail in patients with LL loss [7]. Takemitsu et al [21] measured the muscle content of the trunk in patients with LL kyphosis and found that the strength of posterior extensor muscle was significantly weaker than flexor muscle. Hongo et al. [18] indicated that posterior muscular strength was in correlation to LL loss or kyphosis in the elderly and strengthen lower back musclecould improve LL. Therefore, the restoration of LL by surgery or conservative treatment can increase the muscle volume and improve distribution. At the same time, it emphasizes the importance of strengthening back muscles to improve or maintain the sequance of the spine.
There is a gender-difference in muscle density and CSA in normal populations [4, 22], where the male have greater muscle content than female group, consistent with our data on LCIV in terms of sex. However, this study showed no significance in muscle content in DTLK group, considering the loss of muscle content and lower muscle density in the elderly weakened the gender discrepancy. Consequently, the muscle content and composition must be valued in patients with DTLK or potential DTLK, regardless of aged male or female.
In shows that increased load on spine will lead to loss of intervertebral-space height and reduction of gravity absorbing of disc. Compression on the spine by obesity prolonged, inflammation will be caused through the release of fat cell factors and affect spinal degeneration [23, 24]. In addition, the weakened paravertebral muscles of obese patients and inadequate capacity of maintaining upright will deteriorate intervertebral disc and facet. Wang et al. [3] believed that BMI closely correlated to the formation and progress of degenerative scoliosis, especially BMI ˃25.57 kg/m2 while Kim et al. [25] proposed ambigious attitude. In this study, neither TLK in DTLK group or in control group were not affected by BMI, consistent with the points of Kim et al. There is a significance in muscle content between N and OB sugbroup in control group, indicating that the "obese" figure was also accompanied with "compact" muscle in obese patients and the strength of muscle content was to confrant hyperload on spine with higher BMI [17]. The muscle content was comparable with various BMI but related to TLK severity in DTLK, which mainly because the muscle content of DTLK was more affected by kyphosis than BMI. Meanwhile, the muscle content and strength got lost instead of fat component in DTLK, more obvious in those with larger BMI [26], which was also proved by MRI and intraoperative dissection [27].
The study firstly clarified the characteristics of BMI and paraspinal muscle distribution in DTLK patients by a case-control study. It emphasizd that paraspinal muscle need be paid attention to for DTLK and function excizising or rehabilitation training on paraspinal muscle after surgery was neceseery for promoting the reconstruction of sagittal spinal sequence [28]. Then, the introduction of the LCIV simplified the measurement procedure of paraspinal muscle, saving time and cost for outpatient doctor to make a preliminary judgment and for the patient to perform a self-check [12, 29]. In addition, the study quantified the relationship between TLK, BMI and LCIV. For DTLK patients, measurment on TLK and the muscle content can roughly predict each other, which was valuable for primary diagnosis and taking further measures on DTLK therapy. There were some limitations: Firstly, the measurement of LCIV is not as accurate as CSA, especially for muscle tissue with much FI. Then, the age range so large (50-87y) with no stratification although LCIV was proved stable over 50y that will cause reporting bias. Furthermore, the conclusion was only suitable for patients DTLK with LSS, may not for other types of deformity such as ankylosing spondylitis, Scheuermann's disease or coronal scloliosis. Finally, it was a retrospective study and the points needed to be consolidated by prospective cohort with large sample.