Abstract
Objective
Microdiscectomy is an effective and safe treatment for patients with symptomatic lumbar disc herniation (LDH) that is refractory to conservative interventions. However, some patients experience persistent low back pain (PLBP) after microdiscectomy that is secondary to progressive disc degeneration and segmental instability. This study aimed to clarify the definition of PLBP and analyze its prevalence and associated risk factors.
Methods
This retrospective study included patients who underwent microdiscectomy for LDH at our hospital between 2015 and 2019. We divided this cohort into patients who did (PLBP group) or did not (non-PLBP group) experience PLBP after microdiscectomy and compared their clinical, radiological, and anatomical parameters. We analyzed the relationship between PLBP post-microdiscectomy and the following variables: age, sex, disk herniation level, recurrent disk herniation, body mass index (BMI), modic changes on MRI, facet subluxation, preoperative lumbar pain, and lumbosacral transitional vertebrae (LSTV).
Results
PLBP after microdiscectomy was diagnosed in 99 (29.8 %) of the 332 patients enrolled in this study. Based on our multivariate logistic regression analysis, L5-S1 disc herniation level, recurrent disc herniation after microdiscectomy, obesity, modic changes on preoperative MRI, and facet subluxation were independent risk factors for PLBP post-microdiscectomy. Women and patients aged <50 years showed a trend of increased risk for developing PLBP after microdiscectomy; however, this trend did not reach statistical significance.
Conclusions
PLBP after microdiscectomy is a frequent and understudied condition. We found that an L5-S1 disc herniation level, recurrent disc herniation, obesity, modic MRI changes, and facet subluxation were risk factors for PLBP after microdiscectomy. These results can help surgeons in developing a better understanding of lumbar microdiscectomy outcomes.
Keywords: Low back pain, Microdiscectomy, Lumbar disc herniation, Treatment outcomes, Intervertebral disc
1. Introduction
Lumbar disc herniation (LDH) refers to the bulging of an intervertebral disc into the spinal canal, compressing one or more nerve roots. This causes a clinical syndrome characterized by radicular and lumbar pain and occasional neurological deficits. LDH affects 1–2% of the population and has an incidence of 4.8 per 1000 patient-years [1]. This condition is typical of middle-aged individuals. The initial treatment of choice is medication including anti-inflammatory drugs, along with physiotherapy and postural control [2,3]. LDH is spontaneously reabsorbed in 60–90 % of cases [4,5]. Surgery is recommended only when symptoms persist for more than 4–6 weeks or when a neurological deficit is present [6]. Currently, LDH surgery involves resecting the herniated disc fragment with microsurgical techniques using a minimally invasive approach to the spine, and is termed microdiscectomy [7]. Compared to classical open discectomy, this procedure can be performed through limited skin and fascial incisions, and with limited multifidus muscle detachment. Furthermore, the amount of lamina, ligamentum flavum, and facet joint that needs to be resected is further curtailed by the microsurgical technique. The amount of the intervertebral disc to be resected is limited to the herniated fragment, preserving as much of the normal disc as possible. This minimally invasive procedure is highly effective in resolving pain and allows patients to return to normal work and physical activity sooner [8,9]. Furthermore, this procedure usually has few intra-and postoperative complications [10]. However, some patients complain of persistent low back pain (PLBP) after surgery due to progressive degeneration of the intervertebral disc and segmental instability at the operated level [11,12]. Disc degeneration is a leading cause of lower back pain and is secondary to the loss of proteoglycans [12]. This reduces oncotic pressure and hydration inside the disc [13,14]. With these changes, the nucleus pulposus becomes less resistant to axial loading. The annulus fibrosus is then exposed to abnormal biomechanical stress that triggers an increase in enzymatic activity and collagen destruction [15,16]. Lumbar segmental instability refers to abnormal movement patterns under normal load conditions [17]. Segmental instability is another reported cause of lower back pain [18]. Disc degeneration is the primary cause of lumbar segmental instability [19,20]. Depending on the definition used, the reported PLBP prevalence varies widely between 12 and 75 % [[21], [22], [23], [24], [25]], and significantly affects the quality of life of the patient [21,22]. The previously reported risk factors for PLBP include recurrent lumbar disc herniation (rLDH) and modic changes on magnetic resonance imaging (MRI) (Fig. 1) [1,[26], [27], [28]]. rLDH can be defined as the presence of herniated disc material at the same level in a patient who has experienced a pain-free interval of at least 6 months after surgery [[29], [30], [31]]. Modic changes refer to abnormal endplate signal intensities on MRI [[32], [33], [34]]. Modic changes reflect inflammatory activity in the endplates secondary to the disc degeneration cascade and have been associated with lower back pain [[35], [36], [37], [38]]. PLBP is a recognized complication in clinical practice; however, few reports have focused on it and there is no consensus on its definition and management. We designed this study to analyze the prevalence and risk factors for PLBP in a high-volume spine surgery center. This study was aimed at providing a better understanding of the outcomes of lumbar microdiscectomy.
Fig. 1.
Modic changes. MRI image showing L4-L5 disc herniation and modic changes in L4 (arrow).
2. Materials and methods
This retrospective study included all consecutively admitted patients with LDH who underwent microdiscectomy at the Neurosurgery Department of Virgen de la Arrixaca University Hospital between January 2015 and December 2019. The follow-up period ranged from 1 to 5 years (mean follow-up, 2.5 years). Lumbar MRI was performed on all patients before surgery. LDH levels and end-plate status were assessed on T1-and T2-weighted sequences. Patients with a follow-up of <1 year, more than one-level disc herniation, concomitant degenerative lumbar stenosis, those who needed urgent surgery due to cauda equina syndrome, or required a different surgical technique than microdiscectomy were excluded from this study. PLBP was defined as severe and disabling lower back pain that was refractory to medical treatment, lasted for at least 1 year, occurred after microdiscectomy for LDH, and was associated with disc degeneration. After reviewing the medical records, the enrolled patients were divided into PLBP and non-PLBP groups, and the following variables were compared: age, sex, body mass index (BMI), disc herniation level, modic changes on MRI, recurrent disc herniation, preoperative lumbar pain, facet subluxation (Fig. 2), and lumbosacral transitional vertebrae (LSTV) (Fig. 3). Microdiscectomy was performed by two neurosurgeons using the same approach and the same grade of disc resection. A minimally invasive approach using an operating microscope (OM) was adopted. We systematically performed limited hemilaminectomy, facetectomy, and flavectomy. The herniated disk was resected, leaving the unaffected disk intact. We reviewed the surgical records to identify cases of facet subluxation. Facet subluxation was defined as loss of congruence and an abnormal distance between the facet surfaces in the operated segment. Univariate analysis was performed using Student's t-test and the χ2 test. Multivariate logistic regression analysis was used to identify independent risk factors for PLBP. Any variables with a P value of no more than 0.2 based on a univariate analysis were included in the multiple logistic regression models. Statistical significance was defined as P < 0.05, and statistical analysis was performed using SPSS Statistics software v.24 (SPSS Inc., Chicago, Illinois, USA).
Fig. 2.
Facet subluxation. Interlaminar approach L4-L5 (left side) under the operating microscope. In the image, superior articular process of L5 (A), inferior articular process of L4 (B), ligamentum flavum (C) and facet subluxation (arrow) are shown.
Fig. 3.
Lumbosacral transitional vertebrae (LSTV). MRI image showing a LSTV (arrow) with sacralization of the lowest lumbar vertebral body.
3. Results
A total of 332 patients were included in this study: 181 men (54.5 %) and 151 women (45.5 %), with ages ranging from 18 to 82 years (mean age, 47 ± 12 years). Disc herniation levels were L5-S1 in 182 (54.8 %), L4-L5 in 130 (39.2 %), L3-L4 in 16 (4.8 %) and L2-L3 in 4 (1.2 %) patients. rLDH affected 60 (18.1 %) patients and PLBP had a prevalence of 29.8 %. Facet subluxation was observed in 80 (24.1 %) patients. The characteristics of the study participants are summarized in Table 1. Compared to those without PLBP, patients with PLBP after microdiscectomy had significantly more disc herniations at L5-S1, a higher frequency of modic changes at the disc herniation level, a higher frequency of facet subluxation, a higher prevalence of rLDH, and were significantly more likely to be obese. The characteristics of the study participants, based on the presence or absence of PLBP after microdiscectomy, are summarized in Table 2. Patients with PLBP after microdiscectomy were younger than non-PLBP patients and women were more likely to have PLBP after microdiscectomy. Preoperative lumbar pain and LSTV were more frequent in patients with PLBP after microdiscectomy; however, the differences were not statistically significant. Based on our univariate analysis, the variables included in the multivariate analysis were disc herniation level, modic changes, facet subluxation, rLDH, and obesity (Table 3). Multivariate logistic regression analysis revealed that disc herniation at the L5-S1 level, modic changes, facet subluxation, rLDH, and obesity were independent risk factors for PLBP after microdiscectomy for LDH.
Table 1.
Characteristics of study participants.
| N = 332 | |
|---|---|
| Mean age (yr) | 47 ± 12 |
| Sex (Male:Female) | 181:151 |
| Disc herniation level | |
| L2-L3 | 4 (1.2 %) |
| L3-L4 | 16 (4.8 %) |
| L4-L5 | 130 (39.2 %) |
| L5-S1 | 182 (54.8 %) |
| rLDH | 60 (18.1 %) |
| PLBP | 99 (29.8 %) |
| Obesity | 12 (3.6 %) |
| Modic changes on MRI | 31 (9.3 %) |
| Facet subluxation | 80 (24.1 %) |
| Preoperative lumbar pain | 162 (48.8 %) |
| LSTV | 15 (4.5 %) |
rLDH indicates recurrent lumbar disc herniation; PLBP, persistent low back pain; MRI, magnetic resonance imaging; LSTV, lumbosacral transitional vertebra.
Table 2.
Characteristics of study participants categorized by the presence or absence of PLBP.
| PLBP Group (n = 99) | Non-PLBP Group (n = 233) | OR | 95 % CI | p-valuea | |
|---|---|---|---|---|---|
| Sex (Male:Female) | 53:46 | 128:105 | 0.98 | 0.78-1.21 | 0.815 |
| Mean age (yr) | 46.8 ± 9.5 | 47.9 ± 13.3 | 0.388 | ||
| Disc herniation level | |||||
| L2-L3 | 1 (1 %) | 3 (1.3 %) | 0.94 | 0.53-1.65 | 0.832 |
| L3-L4 | 5 (5.1 %) | 11 (4.7 %) | 1.08 | 0.36-3.18 | 0.898 |
| L4-L5 | 27 (27.3 %) | 103 (44.2 %) | 0.81 | 0.71-0.93 | 0.004 |
| L5-S1 | 66 (66.7 %) | 116 (49.8 %) | 2.17 | 1.29-3.65 | 0.033 |
| rLDH | 34 (34.3 %) | 26 (11.2 %) | 4.17 | 2.33-7.46 | <0.05 |
| Obesity | 10 (10.1 %) | 2 (0.9 %) | 12.9 | 2.79-58.82 | <0.05 |
| Modic changes on MRI | 17 (17.2 %) | 14 (6 %) | 3.25 | 1.53-6.89 | 0.001 |
| Facet subluxation | 32 (32.3 %) | 48 (20.6 %) | 1.84 | 1.09-3.12 | 0.022 |
| Preoperative lumbar pain | 52 (52.5 %) | 110 (47.2 %) | 1.24 | 0.77-1.98 | 0.375 |
| LSTV | 5 (5.1 %) | 10 (4.3 %) | 1.19 | 0.39-3.56 | 0.761 |
OR, odds ratio; CI, confidence interval; rLDH, recurrent lumbar disc herniation; PLBP, persistent low back pain; MRI, magnetic resonance imaging; LSTV, lumbosacral transitional vertebra.
Chi-square test was used for categorical variables, whereas T-test was used for continuous variables.
Table 3.
Summary of significant risk factors for PLBP using multiple logistic regression analysis.
| OR | 95 % IC | p-value | |
|---|---|---|---|
| L5-S1 disc herniation level | 1.61 | 1.03-2.51 | 0.037 |
| Modic changes on MRI | 2.98 | 1.32-6.76 | 0.009 |
| Facet subluxation | 2.07 | 1.16-3.68 | 0.013 |
| rLDH | 3.87 | 2.09-7.17 | <0.05 |
| Obesity | 12.58 | 2.52–62.67 | 0.002 |
OR indicates odds ratio; CI, confidence interval; rLDH, recurrent lumbar disc herniation; MRI, magnetic resonance imaging.
4. Discussion
One of the main difficulties in analyzing PLBP after microdiscectomy is the lack of consensus regarding the definition of microdiscectomy complications. After reviewing the criteria used in other studies [12,[21], [22], [23], [24]], we proposed the following definition for PLBP: severe and disabling lower back pain, refractory to medical treatment, lasting at least 1 year, occurring after microdiscectomy for LDH, and associated with disc degeneration. This retrospective study demonstrated that PLBP is a frequent complication of microdiscectomy for LDH. Our data showed a PLBP prevalence of 29.8 % that is similar to the previously reported range of 14–29.3 % [[25], [26], [27], [28]]. To our knowledge, there have been no reports in the literature that analyzed PLBP as a main objective.
Some risk factors have been reported for PLBP, such as rLDH [22,27,29,30]. rLDH has been associated with PLBP because of the need for repeat microdiscectomy, with additional surgical trauma affecting the damaged intervertebral disc. Moreover, during the second surgery, the interlaminar approach often needs to be expanded. Theoretically, this maneuver can lead to segmental instability. These previous findings are consistent with our present results.
Preoperative lumbar pain is a recognized risk factor for PLBP [26] because microdiscectomy can worsen preexisting intervertebral disc degeneration and segmental instability. However, we did not find any significant association of this variable with PLBP. Our results support the hypothesis that microdiscectomy is effective in treating lumbar and radicular pain secondary to disc herniation [31]. LSTV is a congenital abnormality where the last lumbar vertebra has an elongated transverse process that fuses with the sacrum [32]. LSTV confers abnormal stiffness to the lumbosacral transition and modifies normal biomechanics. Earlier occurrence and more severe disc degeneration have been associated with LSTV in previous studies 45-47. Additionally, LSTV has been associated with PLBP after microdiscectomy [32]; however, we did not find any association between these factors in our study. These results can be explained by the low presence of LSTV in the study participants (4.5 %).
Some reports have shown a higher risk of PLBP in women than in men, probably related to increased joint laxity and a greater tendency towards segmental instability in women [9,33]. Consistent with these earlier reports, our data showed that women developed PLBP after microdiscectomy at a higher frequency than men; however, this trend did not reach statistical significance. A lower tendency to suffer from PLBP has been found in patients older than 50 years in the literature [22] and in our study. We hypothesized that advanced osteoarthritic changes in the intervertebral discs and facet joints, typical of aging, can limit segmental instability and PLBP.
The disc herniation level has been associated with radicular outcomes after microdiscectomy [21]. No studies have examined the relationship between disc herniation level and PLBP. In our study, the L5-S1 level was found to be a risk factor for PLBP. These results can be explained by the special biomechanics of this level as it is the most caudal and is in the lumbosacral transition. The L5-S1 level is considered a segment subject to special biomechanical stress [34] and it can lead to an increased risk of disc degeneration.
Conflicting results have been published in the literature regarding the influence of modic changes in preoperative MRI on microdiscectomy outcomes. Rahme et al. [26] and Ohtori et al. [27] found no links between these variables. However, Barth et al. [35] and Viswanathan et al. [36] described a positive correlation between modic changes and PLBP development after microdiscectomy. Our results showed a significant association between preoperative modic changes at the level of the disc herniation and PLBP. This finding supports the hypothesis that this radiological sign is caused by inflammation that could be the cause of the pain [[32], [33], [34]].
Moreover, the association between obesity and PLBP after microdiscectomy has not been previously described. In our study, a significantly higher risk of PLBP was found in obese individuals, and this could be explained by the mechanical overload in a previously injured intervertebral disc.
During surgery, we observed that some patients did not have congruent facet surfaces at the LDH level, a condition termed facet subluxation. This has been previously reported using dynamic MRIs in 26.3 % of patients with chronic moderate-to-severe LBP without LDH [37]. This is a rare condition in the lumbar spine, even after a traumatic injury [38]. The facets of the lumbar spine are larger and more vertically oriented, providing more resistance to subluxation. Hence, this is a surgical finding that is rarely reported in the lumbar spine, and our study has presented the first reported link between facet subluxation and PLBP after microdiscectomy. We hypothesized that facet subluxation may be related to segmental instability as a source of PLBP. According to Cho et al. [38], facet subluxation requires lesions of the stabilizing ligaments, including the interspinous, supraspinous, and ligamentum flavum.
Few studies have investigated PLBP after microdiscectomy. PLBP is a poorly defined phenomenon that has a significant impact on the quality of life of the patient. To our knowledge, this is the first study to provide a clear definition of PLBP and to analyze the risk factors as its main objective. Understanding these risk factors would be helpful for surgeons and patients to improve their knowledge of lumbar microdiscectomy outcomes.
Our study has some limitations. First, owing to its retrospective design, the data we used were confined to those available from patient medical records. Some variables could not be considered to quantify pain and disability levels, such as the type of microdiscectomy (limited vs. aggressive), Visual Analog Scale, and Oswestry Disability Index. Second, this was a single-center study; therefore, the results should be generalized with caution. Finally, some information on PLBP may have been missed in patients with shorter follow-up periods.
5. Conclusion
We found that PLBP after microdiscectomy is a frequent yet understudied condition. Our data analysis identified L5-S1 level disc herniation, obesity, modic changes on MRI, facet subluxation, and rLDH as risk factors for PLBP after microdiscectomy. Our findings will help surgeons in developing a better understanding of lumbar microdiscectomy outcomes.
Ethical approval
This study was conducted in accordance with the principles of the Declaration of Helsinki. The study protocol was approved by the “Virgen de la Arrixaca” University Hospital Ethics Committee on April 28, 2020 (Ethical Approval Verification Code: CARM-19923b4f-8964-30af-12e2-0050569b6280) and the University of Murcia on June 12, 2020 (Ethical Approval Verification Code: RUxFMv2p-c/Jgg3ib-hRBvtjjI-flx/TDcH).
Provenance and peer review
This article has undergone peer review.
Data availability statement
Dataset includes sensitive or confidential information such as patient data. No web-linked research datasets are available for this study. The data will be made available upon request.
Funding
This study did not require funds.
CRediT authorship contribution statement
Antonio García López: Writing – original draft, Investigation, Formal analysis, Data curation. María-Trinidad Herrero Ezquerro: Supervision, Methodology, Conceptualization. Miguel Martínez Pérez: Supervision, Resources, Data curation.
Declaration of competing interest
None.
Acknowledgements
We thank the Virgen de la Arrixaca University Hospital for sharing their patient database. We also wish to thank the University of Murcia for providing us with data analysis tools.
Contributor Information
Antonio García López, Email: agarcia.med@gmail.com.
María-Trinidad Herrero Ezquerro, Email: mtherrer@um.com.
Miguel Martínez Pérez, Email: miguelmartinezp@gmail.com.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Dataset includes sensitive or confidential information such as patient data. No web-linked research datasets are available for this study. The data will be made available upon request.