Abstract
To investigate the progression of adult spinal process impingement (SPI) and provide a staging system through a retrospective long-term MRI-based longitudinal study. From April 2005 to April 2025, 132 patients who underwent at least four lumbar MRI scans prior to index lumbar surgery were enrolled. The mean follow-up duration was 11.7 ± 3.2 years. Patients were divided into two groups: group 1 (no SPI; n = 70, mean age 60.0 ± 6.4 years, F:M = 45:25) and group 2 (with SPI; n = 62, mean age 67.2 ± 7.1 years, F:M = 43:19). A novel SPI staging system and grading system for herniation of the interspinal ligament (HISL) was established. The analysis focused on the L3/S1 levels. Radiographic assessment included standing anteroposterior and flexion-extension lumbar radiography. Osteoporosis was evaluated using DEXA scans. In group 1, two interspinal ligament patterns were observed: normal MRI (76.7%) and fatty degeneration (23.3%). Group 2 showed 107 SPI levels: 25 at L3/L4, 61 at L4/L5, and 21 at L5/S1 levels. The SPI progresses through four stages: early (I), soft tissue (II), bone (III), and spinal stenosis (IV), with variable intervals. Osteoporosis is a key factor in the development of SPI. HISL appeared in 28 segments of group 2 but none in group 1 (p < 0.001). Of the HISL cases, 12 were mild, 9 were moderate, and 7 were severe. Lumbar decompression was performed in four moderate and five severe cases. This long-term longitudinal MRI study delineated the stages and natural progression of SPI. HISL was strongly associated with the SPI, and its size was the principal factor contributing to spinal stenosis.
Keywords: Herniated interspinous ligament, Spinous process impingement, Baastrup’s disease, Spondylolisthesis, MRI
Subject terms: Anatomy, Diseases, Health care, Medical research, Neurology
Introduction
Adult spinous process impingement (SPI) is defined as “impingement between the spinous processes,” which occurs as part of aging-related degeneration of the lumbar spine1–4. It is generally believed that the prevalence of SPI exceeds 80% in individuals over 80 years of age5–7. Although several studies using MRI have attempted to analyze the SPI, most have been limited to cross-sectional studies. However, the longitudinal progression and clinical significance of the SPI remain poorly understood, underscoring the need for long-term longitudinal studies.
The interspinous ligament (ISL) in the lumbar spine is anatomically oriented in an upward horizontal direction. Functionally, it primarily prevents anterior vertebral displacement and excessive spinal flexion8,9. The ISL is located posteriorly in the spine and positioned between the spinous processes of adjacent vertebrae, similar to the intervertebral disc, which is situated anteriorly between the two vertebral bodies. Pathological changes in the intervertebral disc may lead to herniation, resulting in spinal stenosis and associated symptoms10–12. By analogy, it is reasonable to hypothesize that degeneration may result in anterior herniation of the ISL (HISL) into the spinal canal, potentially causing spinal stenosis. We observed this phenomenon intraoperatively in several dozen patients, and it appeared to occur predominantly in those with SPI. HISL is quite different from ligamentum flavum infoldings, which can be separated during surgery. However, to date, no systematic study has investigated this.
In this study, we aimed to investigate the natural history and classification of adult SPI using a long-term longitudinal imaging analysis. Adult SPI was defined as spinal process impingement due to aging and degeneration of posterior column of spine, which was separated from the youth kissing spine disease due to extreme sports injury. Specifically, we sought to determine whether the SPI contributes to ISL degeneration and protrusion and whether such changes can lead to the spinal stenosis. Our central hypothesis is that SPI-related degeneration of the ISL can result in anterior displacement of the ligament, ultimately causing spinal cord compression and, in some cases, necessitating surgical intervention. To test this hypothesis, we analyzed a cohort of patients with SPI who underwent long-term MRI and radiographic follow-up. We assessed the progression of SPI from the early to advanced stages and established a classification system based on the severity and spinal stenosis. This study aimed to provide a deeper understanding of the pathophysiology of SPI and its clinical significance, potentially guiding future strategies for diagnosis and treatment.
Materials and methods
Collection of image data
This study was conducted in accordance with the principles of the Declaration of Helsinki. and approved by the Ethics Review Board of St. Martin De Porres Hospital, Chia-Yi, Taiwan IRB 24 C-001). Written informed consent was obtained from all individual participants involved in the study and for any accompanying images. Between April 2005 and April 2025, 61,000 lumbar spine MRI scans were performed at our institution. Through an automated selection process, 212 patients who had undergone at least four lumbar MRI examinations before index lumbar surgery were identified. After applying the manual exclusion criteria, eliminating individuals with previous spinal surgery and those diagnosed with spinal tumors or infections, the final cohort of 132 patients remained eligible for analysis. The average age of the study population was 63.3 ± 7.5 years, with a mean follow-up duration of 11.7 ± 3.2 years.
MRI was conducted using different scanner models over the study period: from 2005 to 2020, a 0.3T system (HITACHI Airis2-1, Japan) was utilized, while from 2021 onward, a 1.5T scanner (GE Signa HD28, USA) was employed. Radiographic assessments included standing anteroposterior X-rays, as well as flexion-extension views specifically focused on the fourth lumbar vertebra. These radiographs were supplemented with T1- and T2-weighted MRI sequences to enhance the evaluation of soft tissue structures. The lowest T-score on dual-energy X-ray absorptiometry (DEXA) was used to provide insights into osteoporosis. The average DEXA of all participants was − 2.3 ± 0.6, and the average body mass index (BMI) was 23.0 ± 2.2.
It is associated with spondylolisthesis, disc height loss, or facet joint subluxation, leading to a reduced interspinous space and altered angles between the spinous processes. This was particularly evident in L5 spondylolysis, severe disc degeneration disease (disc space < 3 mm), spondylolisthesis with slippage > 15%, degenerative scoliosis, compression fractures, or combos.
Based on the last standing extension radiographic findings, the 132 patients were classified into two groups. The demographic data are summarized in Table 1.
Table 1.
Demographics of the 132 participants. Quantitative variables are described as mean ± standard deviation (SD).
| Total | No Impingement (Group 1) |
With Impingement (Group 2) |
p-values | |
|---|---|---|---|---|
| Case number | 132 | 70 | 62 | |
| Age (year) | 63.3 ± 7.5 | 59. 9 ± 6.0 | 67.2 ± 7.1 | p = 4.6*10−9 |
| Female:Male | 88:44 | 45:25 | 43:19 | p = 0.58 |
| DEXA T-score | − 2.3 ± 0.6 | − 2.0 ± 0.5 | − 2.7 ± 0.6 | p = 2.9*10–11 |
| BMI | 23.0 ± 2.2 | 23.2 ± 2.1 | 22.7 ± 2.2 | p = 0.16 |
| Follow-up duration (year) | 11.7 ± 3.7 | |||
Group 1: Patients without SPI (n = 70) with a mean age at the first MRI scan of 59.9 ± 6.0 years and a female-to-male ratio of 45:25. The average DEXA was − 2.0 ± 0.5; BMI, 23.2 ± 2.1.
Group 2: Patients with SPI (n = 62) with a mean age at the first MRI scan of 67.2 ± 7.1 years and a female-to-male ratio of 43:19. The average DEXA was − 2.7 ± 0.6; BMI, 22.7 ± 2.2.
Classification of SPI and ISL
Based on Keorochana’s classification13, ISL on MRI images was categorized into four grades: Grade 1: low- to iso-signal intensity on both T1- and T2-weighted images, that is, the normal stage. Grade 2: High signal intensity on both T1- and T2-weighted images, indicating fat degeneration. Grade 3: Low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, that is, the soft tissue stage. Grade 4: Low or iso-signal intensity on both T1- and T2-weight images with marked narrowing of the interspinous distance, that is, degenerative ISL without fat infiltration.
In Group I, there was no SPI, as confirmed by the last extension view. All subsequent evaluations were based on serial longitudinal MRI scans, according to Keorochana’s classification. In Group 2, because the SPI was confirmed by the last extension view, the following criteria were used to stage the SPI (Table 2):
Table 2.
Staging system of SPI.
| Definition & criteria | Extension view—T2 MRI—T1 MRI | |
|---|---|---|
|
Stage 1 Early stage |
Extension view with SPI with normal ISL MRI signal |
|
|
Stage 2 Soft tissue inflammation stage |
T2 hyper-signal T1 hypo-signal No SP bone pathology |
|
|
Stage 3 Bony pathological stage |
Bone erosion or micro-fractuSre in the impingement region, bone cystic formation, or pseudarthrosis |
|
|
Stage 4 Spinal stenosis stage |
≥ grade 1 Herniated ISL with spinal stenosis |
|
Stage I: Early stage. If there were no bone changes with a normal ISL MRI signal, an early stage was assigned14,15. In the initial phase, the patients experienced mild back pain or stiffness. Typically, no specific treatment is required for this condition.
Stage II: Soft tissue inflammation stage. If there were no bone changes or HISL with low signal intensity on T1-weighted images and high signal intensity on T2-weighted images on MRI scans, it was assigned to the soft-tissue stage. In the initial phase, patients experienced mild-to-moderate back pain or stiffness. Patients in this group usually need to take medicine or wear back braces while working. In our study, none of the patients remained in this stage for a long period. After long-term follow-up, all patients progressed to the bone or neural stages.
Stage III: Bone pathological stage. If any bone changes were observed on serial MRI, including bone erosion or microfracture in the impingement region, bone cystic formation, or pseudarthrosis between the spinous processes, and there was no ≥ grade 1 HISL, the bone stage was assigned. In our study, 21 of the 54 patients with bone-stage disease finally progressed to the neural stage.
Stage IV: Spinal stenosis. Previously, in the soft tissue (2 cases) or bone stages (21 cases), once HISL equal to or greater than grade 1 was identified, leading to encroachment of spinal canal, spinal stenosis stage was assigned. In this study, nine of the 23 patients underwent decompression surgery.
Classification of HISL
The HISL classification divides the spinal canal into four equal sections based on midsagittal MRI findings14. The boundary between the ligamentum flavum and the ISL was not clearly defined in the MRI transverse axial view, making the classification impossible to use in axial views. In contrast, the ligamentum flavum is clearly differentiated from the ISL on sagittal MRI. The ligamentum flavum has an off-centric distribution with a worm-like shape, and the ISL is in the midsagittal region with a cone shape and a sharp end pointing to the spinal cord. This classification assesses the extent of posterior-to-anterior compression caused by the protruding ISL and categorizes the severity into three grades:
Grade 0 (asymptomatic): posterior dural indentation ≤ 25%, regarded as normal degeneration.
Grade I (mild): posterior dural indentation between 26% and 50% of the spinal canal width on midsagittal MRI with mild neurological symptoms, including numbness or soreness of the bilateral lower limbs.
Grade II (moderate): Significant spinal canal narrowing between 51% and 75%, often associated with moderate clinical spinal stenosis symptoms, including lower limb numbness, soreness, or intermittent claudication.
Grade III (severe): Severe spinal canal compromise > 75%, typically resulting in marked neurological symptoms, including lower limb numbness, soreness, intermittent calculation, and voiding or bowel dysfunction. Surgical intervention may be required.
This classification aids in the assessment of spinal stenosis severity and guides treatment decisions, ranging from conservative management to surgical intervention, when necessary.
Missing data
Ten patients did not have final DEXA data available. To address this, we used our existing database to identify 10 subjects matched for sex, age, and BMI (within ± 1.0), and used the average DEXA values of these matched individuals as the estimated values.
Statistical analysis
The differences in age, female: male ratio, DEXA T-score, and BMI in terms of demographic information and biochemical data were examined using Student’s t-test (Table 1). Multivariate logistic regression analysis was performed to identify factors independently associated with group 2 status. The variables entered into the model included pars fracture, listhesis, degenerative disc disease, degenerative scoliosis, compression fracture, and combined pathology. All variables were entered simultaneously to evaluate their independent effects on the outcome variables. The results are reported as adjusted odds ratios (ORs) with 95% confidence intervals (CIs). A two-sided p-value < 0.05 was considered statistically significant (Table 3).
Table 3.
Multivariate logistic regression analysis for factors associated with group 2.
| B | S.E. | Wald | df | Exp (B) | 95% CI for EXP (B) | p-values | |||
|---|---|---|---|---|---|---|---|---|---|
| Lower | Upper | ||||||||
| Step 1a | L4 or L5 pars fracture (1) | 1.657 | 1.285 | 1.661 | 1 | 5.241 | 0.422 | 65.103 | p = 0.198 |
| Spondylolisthesis (1) | − 1.244 | 0.487 | 6.519 | 1 | 0.288 | 0.111 | 0.749 | p = 0.011 | |
| Severe DDD (1) | − 0.485 | 0.484 | 1.003 | 1 | 0.616 | 0.239 | 1.590 | p = 0.317 | |
| Degenerative scoliosis (1) | − 1.913 | 0.840 | 5.180 | 1 | 0.148 | 0.028 | 0.767 | p = 0.023 | |
| Compression fracture (1) | 0.049 | 0.905 | 0.003 | 1 | 1.050 | 0.178 | 6.192 | p = 0.957 | |
| Combo (1) | − 1.919 | 1.420 | 1.828 | 1 | 0.147 | 0.009 | 2.371 | p = 0.176 | |
| Constant | 0.644 | 0.263 | 5.977 | 1 | 1.904 | p = 0.014 | |||
aVariable(s) entered on step 1: pars fracture, listhesis, DDD, degenerative scoliosis, compression fracture, and combo.
Number of patients: n = 132. Model likelihood ratio test: p = 0.0137.
To ensure the reliability of the measurements, 20% of the samples were randomly selected for re-measurement by the primary investigator (to assess intra-observer reliability) and by a second independent researcher (to assess inter-observer reliability) after a two-week interval. The details of the intra- and inter-observer error analyses for all parameters are summarized in Table 4. The threshold for statistical significance was defined as a two-sided p-value of ≤ 0.05. Statistical Package for the Social Sciences, version 18.0 (SPSS Inc., Chicago, IL, USA) for Windows was used for the statistical analyses.
Table 4.
The intra- and inter-observer error analysis of the four SPI stage evaluation criteria (ICC: intraclass correlation coefficient. CI: confidence interval).
| SPI stage | Intra-observer ICC (95% CI) |
Inter-observer ICC (95% CI) |
|---|---|---|
| Early stage | 0.91 (0.87–0.94) | 0.88 (0.84–0.92) |
| Soft tissue inflammation stage | 0.89 (0.85–0.93) | 0.86 (0.82–0.90) |
| Bony pathological stage | 0.88 (0.85–0.90) | 0.87 (0.82–0.91) |
| Spinal stenosis stage | 0.85 (0.82–0.88) | 0.90 (0.88–0.92) |
Results
The intra- and inter-observer reliabilities were excellent (Table 4). The Intra-observer ICCs of the four SPI stage evaluation criteria ranged from 0.85 (spinal stenosis stage) to 0.91 (early stage). The Inter-observer ICCs ranged from 0.86 (soft tissue inflammation stage) to 0.90 (spinal stenosis stage).
Groups 1 and 2
Multivariate logistic regression analysis demonstrated that listhesis (adjusted OR 0.29, 95% CI 0.11–0.75, p = 0.011) and degenerative scoliosis (adjusted OR 0.15, 95% CI 0.03–0.77, p = 0.023) were independently associated with group 2 status. Pars fractures showed a trend toward association but did not reach statistical significance. Other variables were not significantly associated with this outcome after adjustment.
Two distinct patterns of interspinous ligament changes were observed in 70 patients without impingement syndrome. Degeneration of ISL (Keorochana grade 4): gradual narrowing of the interspinous space on radiographs with normal MRI ISL signals; the tail of the spinous process enlarged over time, leading to significant narrowing of the interspinous space in the tail region, although narrowing in the spinous body region was less pronounced. MRI revealed consistently low or iso T1- and T2- weighted signals, without significant changes. The frequencies of the cases were 161 segments (76.7%), and the distribution was 56 L3/L4, 58 L4/L5, and 47 L5/S1.
Fatty Degeneration of ISL (Keorochana grade 2): progressive fat infiltration into the ISL. MRI revealed consistent hypersignals on both T1- and T2-weighted images, and the fat area gradually increased. The frequencies of cases were 49 segments (23.3%) and the distribution was 14 L3/L4, 16 L4/L5, and 19 L5/S1.
Among the 62 patients, 107 segments showed SPI. The distribution was as follows: 25 segments at L3/4, 61 segments at L4/5, and 21 segments at L5/S1 level. In terms of patient distribution, one patient had an SPI at L3/4, 20 at L4/5, 20 at L3/5, 17 at L4/S1, and four at L3/S1. The progression was categorized into four stages (Figs. 1, 2, 3 and 4). The final stage distribution was stage I (8 levels in 6 patients, 63.2 years,7.5%), stage II (0 levels in 0 patients, 0%), stage III (71 levels in 33 patients, 66.3%), and stage IV (28 levels in 23 patients, 26.2%). The time intervals between the stages varied considerably. The distribution of HISL was as follows: six segments at L3/4, 17 segments at L4/5, and five segments at L5/S1. In contrast, among the 70 cases in group 1 (i.e., 210 levels without SPI), none exhibited ≥ grade 1 HISL (p < 0.001). The grading of spinal stenosis due to HISL was as follows: mild, 12 levels in 10 patients; moderate, 9 levels in 8 patients; and severe, 7 levels in 5 patients. Lumbar decompression surgery was performed in five (62.5%) moderate and four (80%) severe cases.
Fig. 1.
A 56-year-old male was diagnosed with an L5 pars fracture causing an SPI between L4 and L5. Initial MRI showed L4/5 SPI stage II without nerve compression, and the symptoms were limited to work-related back pain. MRI performed 11 months after the initial imaging evaluation revealed progression to SPI stage IV with grade 2 HISL, leading to spinal canal stenosis and bilateral leg numbness during walking.
Fig. 2.
A 75-year-old male patient. On the first MRI, an SPI stage II was observed at the L3/L4 level. Six months later, bony changes developed and progressed to stage III. After another year, HISL was observed, indicating progression to stage IV. The L4/L5 level was already at stage III on the initial MRI and eventually progressed to stage IV.
Fig. 3.
A 68-year-old female with L4/5 SPI. The first MRI showed that it was at stage I. After three years and 5 months, it progressed to stage III, and after another two and a half years, it developed into stage IV with HISL.
Fig. 4.
A 79-year-old male who underwent six MRI scans over a period of seven years. The images show progression at the L4-L5 SPI, starting from stage I, advancing to stage III, and eventually reaching stage IV within 7 years. Additionally, fatty degeneration is observed at the L5-S1 level.
There were accompanying diagnoses in our subjects, including three L5 pars fractures, 14 disc degenerative diseases, 20 spondylolistheses, eight degenerative scoliosis, two compression fractures, and five with two of them. There was a small subgroup consisting of only five cases in which none of the above-mentioned diagnoses were present. In this subgroup, eight spinal levels demonstrated SPI, among which three levels developed HISL, all classified as Grade I–II. The mean age of the patients was 71.1 ± 5.6 years. The mean DEXA T-score was − 2.9 ± 0.3. Age and osteoporosis were similar to stage III.
Natural history and variable progression
The timeline and trajectory of SPI progression varied significantly and are summarized in the flowchart (Fig. 5).
Fig. 5.
Flowchart of SPI progression with staging.
Based on our observations, patients may remain asymptomatic in stage I for 1–12 years. From there, the condition may follow one of two primary pathways: In younger or more active individuals (62.8 ± 7.5 years, female and male ratio 1:4 with DEXA − 2.1 ± 0.7), that is, with good bone quality to resist bone erosion and relatively heavy work with repeated impingement, SPI stage I may progress into the stage II and then, bypassing the stage III, directly proceed to stage IV. In some patients with poor bone quality and still energetic activities (68.1 ± 7.0 years and female and male ratio 38:13 with DEXA − 3.0 ± 0.5), stage I impingement may directly induce spinal process bone edge erosion and directly advance into stage III without entering stage II.
Outcomes of stage II
If SPI progresses to the soft tissue stage (62.8 ± 7.5 years, female-to-male ratio of 1:4 with DEXA − 2.1 ± 0.7), two different clinical courses are possible.
Directly progressing to stage IV (56.5 ± 2.1 years, female: male ratio 0:2. with DEXA − 1.3 ± 0.3) (Fig. 1). Anterior protrusion of the interspinous ligament may cause severe spinal stenosis, resulting in a rapid transition to stage IV disease.
Progression to bone stage (67.0 ± 6.6 years, female: male ratio 1:2 with DEXA − 2.6 ± 0.2) (Fig. 2). Continued mechanical stress and inflammation lead to spinous process degeneration, initiating stage III and finally advancing to stage IV disease. No patient remained in the simple stage II at the final follow-up visit.
Outcomes from the stage III
Two outcomes are possible in Stage II.
Progression to stage IV (Figs. 2 and 3): After a period of structural deterioration, extrusion of the interspinous ligamentous tissue may eventually cause spinal stenosis and transition to stage IV.
-
2.
It stays in stage II for a long time (Fig. 4). The time intervals between HISL grades varied significantly. Because MRI scans were not regularly performed, the actual beginning date of each grade could not be accurately detected. Based on our observations, HISL progression from grade 1 to grade 3 may last from 6 months to 8 years.
The location of the HISL was related to the associated diagnosis: same levels in 20 spondylolisthesis cases, upper adjacent level in 3 pars fractures, and 14 severe disc degeneration disease (DDD) cases (p < 0.001).
Discussion
The present longitudinal study of SPI focuses on the development and serial changes in the same subjects over a period and attempts to explore the natural course of progression and staging systems. First, two distinct subtypes of ISL degeneration were identified in group 1 without SPI: aging and fat degeneration. This study proposes a staging system for SPI, which includes early, soft tissue, bone, and spinal stenosis stages. The presence of HISL correlated with dural compression and was significantly associated with SPI (p < 0.001). However, its occurrence at levels without SPI was not observed in this study. The distribution of HISL was correlated with the underlying pathology, occurring at the same level in spondylolisthesis and at the upper adjacent level in cases of pars fractures and severe degenerative disc disease (p < 0.001). These findings suggest that SPI is a critical factor in HISL development, and its progression is influenced by mechanical stress over time. Finally, the spinal conditions associated with SPI were analyzed, and the three major factors were disc degenerative diseases, spondylolisthesis, and degenerative scoliosis.
Interpretation of multivariate findings
The present study identified listhesis and degenerative scoliosis as independent factors associated with group 2 status after adjustment for multiple degenerative pathologies. These findings suggest that spinal instability and structural deformity may play a more important role in disease progression than isolated degenerative changes. Listhesis reflects underlying segmental instability, which may lead to abnormal load transmission and repetitive micromotion. Degenerative scoliosis is a global deformity characterized by asymmetric loading and multiplanar imbalance, potentially amplifying localized degenerative processes. Although pars fractures demonstrated a directional association, statistical significance was not reached, possibly due to the limited sample size; however, the magnitude of the observed effect suggests potential clinical relevance.
HISL in Pars fracture and degenerative lumbar conditions
In cases of pars fracture, the posterior elements, including the spinous process, remain in place owing to the stabilizing effect of the ligaments and muscles, while the vertebral body gradually translates anteriorly. This anterior displacement increases mechanical stress on the intervertebral disc, leading to progressive DDD and disc height reduction. Despite this, the facet joints often maintain a near-normal height, resulting in anterior and inferior tilting of the vertebral body. Consequently, the spinous process of the affected vertebra moves superiorly and collides with the spinous process of the segment above, leading to an SPI. This impingement forces the ISL anteriorly into the spinal canal and contributes to central stenosis16. For example, in cases of an L5 pars fracture, HISL typically occurs at the L4/5 level. Similarly, an L4 pars fracture leads to HISL at L3/4, whereas an L3 pars fracture results in HISL at L2/3.
In advanced DDD, if the facet joint height is relatively preserved, the anterior vertebral tilt becomes pronounced. This leads to the upward migration of the posterior elements, increasing the likelihood of SPI at the superior adjacent level. Consequently, the ISL is pushed anteriorly into the spinal canal, causing HISL.
In cases of spondylolisthesis, the combination of facet joint subluxation and intervertebral disc height loss reduces the distance between adjacent spinous processes, increasing the likelihood of SPI at the same level and subsequently leading to a HISL.
SPI stage III and its relationship with HISL
Our study found that 23 (70.2 ± 7.6 years, female-to-male ratio 15:6, with DEXA − 2.9 ± 0.5) of 56 patients with SPI bone stage advanced into the neural stage with HISL. Typically, bone stages occur in older individuals with osteoporosis, making them more susceptible to this condition than younger individuals. Once the bone stage develops, the junction between the ISL and bone is compromised, and ISL-bone separation may be induced step-by-step, leading to complete detachment. Consequently, when the SP is compressed, it further pushes the ISL anteriorly into the spinal canal, leading to HISL17–21. Furthermore, a reciprocal relationship exists between the ISL migrating anteriorly and the SPs losing their stabilizing structures, which increases bone-on-bone contact. This leads to progressive bony destruction, exacerbating the severity of the bone stage. This explains the high incidence of HISL in the bone stage and why HISL is frequently observed in patients in the bone stage.
The HISL severity and the size of ISL
The severity of HISL is closely related to the size of the ISL. Our study found that most cases of HISL remained at grades 0 or 1, with severe cases being relatively uncommon. Further analysis revealed that in older patients, the ISL undergoes wear and degeneration, resulting in a reduction in size15,16,22,23. Consequently, even if the ligament protrudes, the extruded volume is relatively small, resulting in less severe compression. However, in younger patients, particularly those in their 50s, the ISL remains larger and structurally intact. Similarly, at the L2/3 level, where the ISL is naturally larger, extrusion can result in a more significant compression. Therefore, the severity of HISL is strongly associated with the initial size of the ISL. In general, as age increases, the ISL tends to become degenerated and smaller, leading to less severe compression.
Clinical symptoms of HISL in SPI
In this study, the presence of HISL in patients with SPI did not necessarily indicate the onset of symptoms. Because HISL compression originates from the posterior aspect of the dural sac and does not directly impinge on the nerve roots, the symptoms were more similar to those of spinal stenosis. HISL grade 0 is symptomless. Symptoms appear only when HISL progresses to grade 1–3. Stenosis symptoms become more significant when HISL occurs concurrently with ligamentum flavum hypertrophy or intervertebral disc herniation (Fig. 6). Therefore, when performing endoscopic or other minimally invasive decompression surgeries, it is crucial to remove the ISL to prevent the possibility of requiring a second surgery in the future.
Fig. 6.
Spinal stenosis can be attributed to the following primary factors: (1) thickening of the ligamentum flavum, (2) facet joint hypertrophy, (3) HISL, and (4) additional contribution from the bulging disc.
Limitations
This retrospective study had several inherent limitations that must be considered when interpreting our results. First, there was no fixed time between the MRIs for these patients, and the actual starting date of each grade could not be accurately detected. Second, all clinical information regarding the symptoms of these patients was based only on medical records, which may not be as detailed as required. Third, the DEXA data could only partially provide insights into bone quality, and no CT data were available. Fourth, causality was not the major aim of this study; all speculations of mechanisms may require further studies in the future. Additionally, inter-observer variability in the interpretation of radiographic imaging, particularly X-rays and MRI, could influence the consistency of the assessments. Future prospective multicenter studies with larger cohorts are necessary to further substantiate these findings and enhance their clinical applicability.
Conclusions
A long-term longitudinal study could further elucidate the natural course and progression of the SPI. The 4-staging system of SPI included early, soft tissue, bone, and neural stages. SPI was observed in 107 segments, mostly at L4/5, with 28 HISL levels. HISL was strongly associated with SPI (p < 0.001) but rarely occurred in the absence of SPI. Most cases of HISL advance from the SPI bone stage. The HISL location correlated with the underlying pathology. Osteoporosis is an important factor in the development and progression of SPI.
Author contributions
Kung-Chia Li performed the surgery and organized the structure of this study and coordinated the draft of the manuscript. Ching-Hsiang Hsieh, Ting-Hua Liao, and Yu-Kun Xu participated in the surgery and data collection. Kung-Chia Li and Shang-Chih Lin performed critical revisions of the final manuscript. All authors have checked and approved the final manuscript.
Funding
No Funding.
Data availability
The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.
Declarations
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Kung-Chia Li and Shang-Chih Lin have contributed as Co-first author.
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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
The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.






