Study on the pathogenesis of AS
The pathogenesis of AS remains uncertain, although it is widely accepted that multiple factors contribute to its occurrence [
19‐
21]. Chen Chao et al. [
22] suggested that axial symptoms may be related to damage to the posterior cervical ligamentous complex and small joint degeneration. Changes in cervical biomechanical properties after surgery disrupt normal biomechanical balance, leading to tension in damaged muscles, ligaments, and joint capsules, which stimulates pain receptors, ultimately causing clinical symptoms such as fatigue and pain. Z Liang et al. [
23] found that preoperative inflammatory factors are often in an activated state in patients with axial symptoms, suggesting a lower inflammatory threshold. Severe damage to muscles, ligaments, and small joints during surgery may further activate inflammatory factors in peripheral nerve fibers, exacerbating the inflammatory response, and leading to pain and muscle spasms.
Risk factors of AS
This study has revealed that the preoperative anterior encroachment rate on the spinal canal is a risk factor for the occurrence of AS, which aligns with the findings of Yusof and Naruse et al. [
24,
25]. A higher preoperative anterior encroachment rate puts the spinal cord under prolonged compression, leading to potential damage and necrosis of the autonomic nerves that supply the blood vessels in the neck and shoulders. Consequently, this can result in symptoms such as neck and shoulder pain, numbness, and stiffness. Additionally, the limited space for posterior spinal cord movement may cause tension on connecting structures like the dentate ligament, leading to muscle fatigue and axial symptoms, including reduced sensation, pain, and limited mobility in the neck and shoulder regions. This study identified a cutoff value of 28.5% for the preoperative anterior encroachment rate, suggesting that when it exceeds 28.5%, there is a higher likelihood of AS development postoperatively. Thus, for patients with a preoperative anterior encroachment rate greater than 28.5%, postoperative rehabilitation therapy combined with neurotrophic medications may be considered for preventive treatment to reduce the incidence of AS.
The C7 spinous process plays a crucial role as an insertion point for the ligamentum nuchae, trapezius, and rhomboid muscles, contributing to the stability of the cervical spine. Previous studies, including Ono et al. [
26] who conducted anatomical research on 50 cadavers, have confirmed that preserving the C7 spinous process effectively reduces muscle infiltration in the neck region. Lin W et al. [
27], in a randomized single-blind controlled trial involving 96 patients, found that preserving the C7 spinous process better maintained cervical spine mobility and alignment in the sagittal plane, reduced blood loss, and lowered the incidence of axial symptoms. Hosono et al. [
28] prospectively reduced the range of LP from C3–7 to C3–6, and found that the incidence of AS was significantly reduced after C3-6 laminoplasty (5.4% vs. 29%,
P = 0.015). Consistent with prior research, this study also identified that intraoperative disruption of the C7 spinous process insertion point is a risk factor for the occurrence of AS following lumbar puncture. Therefore, it is essential to protect the integrity of the C7 spinous process insertion point during surgery.
Another risk factor for AS development is damage to the facet joint. Prior research indicates that detachment, necrosis, and scarring of the soft tissues around the facet joint are closely associated with postoperative AS, and approximately 40% to 55% of chronic neck pain is related to facet joint issues [
29,
30]. This may result from surgical stimulation of the posterior nerve branch nerve receptors, and joint surface damage during surgery could lead to aseptic inflammation, causing persistent neck pain. Hence, both suture and traction of the facet capsule can contribute to the occurrence of AS after lumbar puncture, requiring special attention to maintaining the integrity of the facet joint capsule during the procedure.
Studies have shown that the more intact the preservation of posterior neck muscles and ligaments postoperatively, the lower the incidence of AS [
31,
32]. When the preoperative cervical curvature is insufficient, patients often experience discomfort in the neck and shoulder regions, leading to compensatory loss of physiological lordosis in the cervical spine. To maintain sagittal plane mechanical balance, the muscles and ligaments are subject to prolonged contraction and fatigue, leading to atrophy and degeneration, ultimately resulting in axial symptoms such as neck and back pain. Therefore, a larger preoperative cervical curvature serves as a protective factor against AS development, and when the preoperative cervical curvature is less than 16.5°, there is a higher risk of AS postoperatively. Moreover, substantial loss of cervical curvature is also a risk factor for AS occurrence since significant and rapid loss of curvature can lead to local structural disruptions, causing localized symptoms due to poor adaptation. Furthermore, a significant decrease in cervical mobility is also a risk factor for AS development. Previous research has indicated that the loss of cervical mobility may not be the cause but rather a consequence of axial pain, where axial pain restricts cervical movement [
33]. However, this study administered X-ray and CT examinations to AS patients after taking nonsteroidal anti-inflammatory drugs (Gabapentin 0.3 g tid po) for temporary pain relief and found that the degree of cervical mobility loss in Group A remained higher than in the non-AS group. The difference between the two groups was statistically significant, leading to the belief that a significant loss of cervical mobility is a risk factor for AS development.
Anatomical research has shown that due to the unique anatomical structure of the cervical spine, it is challenging to directly address compression on the dura mater anteriorly during lumbar puncture surgery, relying solely on the “bowstring” principle for indirect decompression [
34]. The degree of laminectomy determines the space available for posterior spinal cord drift. A larger laminectomy angle provides more drift space and better recovery of neurological function. However, a larger laminectomy angle also increases the asymmetry of the cervical posterior bony structures, resulting in increased traction on the small joint capsules. Additionally, it can cause separation of paraspinal muscles from the lamina, leading to muscle atrophy. Furthermore, a larger laminectomy angle leads to increased posterior spinal cord drift distance, resulting in nerve root traction within the osseous fibrous canal, causing axial pain. Therefore, the laminectomy angle is considered a risk factor for AS development.
Finally, we found that early postoperative functional exercises are another protective factor against AS occurrence. Early scholars commonly believed that postoperative stability in the cervical spine was poor and discouraged early neck muscle exercises for patients [
35]. However, clinical observations have shown that early active flexion–extension exercises of the neck after surgery effectively prevent atrophy of the posterior neck muscles and excessive scar tissue proliferation, significantly reducing the occurrence of stiffness and pain in the neck postoperatively [
36,
37]. This study suggests that early postoperative functional exercises significantly reduce the incidence of AS. Therefore, it is necessary to perform early neck muscle exercises based on each patient's condition, especially for those with good wound healing and no significant complications, starting two weeks post-surgery.
Shortcomings
However, this study has several limitations that need to be acknowledged. Firstly, it is a single-center retrospective study, and though we have attempted to include a sufficient number of risk factors, there might still be some potential risk factors that were not considered, for instance, the BMI, the degree of the disk degeneration before the surgery, etc. In addition, while the study has identified the risk factors for AS development, some of these factors have not been further quantified, such as the specific degree of laminectomy angle. Furthermore, the obtained ROC-AUC values for certain critical cutoff points of risk factors in this study are still relatively low, casting doubt on the practical feasibility of their clinical application. Lastly, the follow-up duration for some patients was relatively short, and more extended, long-term follow-up is necessary to ascertain specific outcomes. Therefore, future research should focus on conducting multi-center studies with larger sample sizes and longer follow-up periods to further validate and expand upon our findings.