Ligamentum flavum hypertrophy significantly contributes to the severity of neurogenic intermittent claudication in patients with lumbar spinal canal stenosis

Abstract

Ligamentum flavum hypertrophy (LFH) is a known contributor to lumbar spinal canal stenosis (LSCS). However, the clinical significance and quantitative role of LFH compared to other components, such as disc bulging and facet hypertrophy, have not yet been examined. We investigated the correlation between the quantitative radiological factors, clinical symptoms, and outcomes in patients with LSCS. In total, 163 patients diagnosed with single-level (L4-L5) stenosis were included. The patients were divided into 2 groups according to claudication severity: >100 m for mild (n = 92) and < 100 m for severe (n = 71). The visual analog scale (VAS) was used to quantify back and leg pain, and the Oswestry Disability Index (ODI) and Short form-36 (SF-36) physical component summary (PCS) scores, and Macnab criteria were evaluated as clinical factors 6 months after treatment. We measured the baseline canal cross-sectional area, ligamentum flavum (LF) area, disc herniation area, dural sac area, fat area, and LF thickness using MRI. A comparative analysis was performed to evaluate the association between radiologic and clinical factors. Additionally, further comparative analyses between the types of surgeries were performed. Among various radiologic factors, the baseline LF thickness (odds ratio [OR] 1.73; 95% confidence interval [CI] 1.25-2.41) was the only major contributing factor to the severity of claudication in the multivariate logistic regression analysis. The types of surgery (decompression alone vs fusion) did not significantly differ in terms of their clinical outcomes, including back and leg VAS, ODI, SF-36 PCS, and satisfaction with the MacNab classification. LF thickness is a major factor contributing to claudication severity.

Ligamentum flavum analysis in patients with lumbar discus hernia and lumbar spinal stenosis

“…On the other hand, the symptoms are relieved by forward exion, sitting, or recumbence. It is recently postulated that in ammatory changes contribute to LF hypertrophy, or that in ammation by itself causes neurogenic claudication's and pain [11][12][13]. In our study histological changes of LF are investigated in two different groups after which proposition for new mechanism of neurogenic claudication's was obtained.…”

Lumbar Spinal Stenosis and Minimally Invasive Lumbar Decompression: A Narrative Review

“…13 Regarding the mechanism of the dynamic component of LSS, several articles have reported that posture-induced or axial pressure-induced elastic deformation of LF was the main contributor. [14][15][16][17][18][19][20][21] Lumbar extension or standing position may cause two adjacent laminas to move closer, followed by LF thickening and infolding. By contrast, lumbar flexion or lying flat position may cause the two-adjacent lamina to separate, resulting in the stretching and thinning of LF as well as the disappearance of LF infolding.…”

Ligamentum flavum analysis in patients with lumbar discus hernia and lumbar spinal stenosis

“…In contrast, the venous stasis theory suggests that a combination of low levels of oxygen and metabolite buildup are responsible due to venous backup at the cauda equina. It is recently postulated that inflammatory changes contribute to LF hypertrophy, or that inflammation by itself causes neurogenic claudication's and pain [7][8][9] . In our study histological changes of LF are investigated in two different groups after which proposition for new mechanism of neurogenic claudication's was obtained.…”