The “Thickened” Ligamentum Flavum: Is It Buckling or Enlargement?

Discussion

There is uncertainty as to whether apparent thickening of the LF is due solely to loss of disk space height and subsequent LF buckling or whether LF thickening may be present in the absence of an abnormal disk space. To address this issue, we examined 2 cohorts of patients (groups 2 and 3). Both groups had LF thickening and FH; however, only group 3 also had intervertebral disk-height loss at L4–5.

Besides the often-observed buckling of the LF, reports in the literature also ascribe LF thickening to other factors such as mechanical stress and physical activity levels.^5,6 Increasing patient age has been shown to correlate with LF thickening at the L4–5 level,^6,7 presenting as young as 30 years of age in 1 recent study⁸; however, Safak et al⁹ have recently found no such association.

Additionally, even though buckling of the LF secondary to intervertebral disk-height loss has often been cited,^1–3 LF thickening has also been associated with FH changes,⁴ which, in association with other findings, contributed to lumbar spinal stenosis, sometimes in the absence of DDD.⁸ Our results not only support these observations and our primary hypothesis but suggest that there may also be an independent relationship between intervertebral disk height and LF thickening. This is especially true in the few contrast-enhanced studies that showed asymmetric FH associated with ipsilateral LF thickening and enhancement.

In patients with spinal stenosis, Park et al⁵ found a mean thickness of the LF of 4.44 mm, thicker than the LF thickness in the control group (2.44 mm). Other studies have shown normal thicknesses of the LF, ranging from 1.8 to 5 mm.^4,9–11 Our results for normal LF thickening, showing a mean of 3.1 mm, are similar to the findings in these studies.

Moreover, our findings and observations strengthen the secondary hypothesis of this study that inflammatory changes may be an inciting factor for LF thickening. Histologic studies have found that fibrocartilaginous transformation provoked by collagen proliferation and ossification can lead to LF thickening.^6,12 Age-related fibrosis or decrease in the elastin-to-collagen ratio, in combination with biomechanical stress, has been reported to lead to thickening of the LF.^5–7 Pathologic studies have revealed leakage of inflammatory cytokines from degenerating facet joints, implicating these molecules as causes of both LF thickening and pain generation in the adjacent nerve fibers.^13,14 Additionally, Sairyo et al¹⁵ have found LF thickening to be a result of scarring from inflammation, prompted by mechanical stress-induced tissue damage.

As a corollary, we also found that in cases of asymmetric LF thickening, both the thickness and postcontrast enhancement were greater on the side harboring the more severe facet degeneration (Figs 4 and 5). This finding implies a spatial and causal relationship between facet degenerative changes and LF thickening.

Careful and systematic evaluation of facet joints and the LF is important. Specifically, recognition of the correlation and possible causal relationship between FH and LF thickening can facilitate detailed and relevant evaluation of the cause of lumbar spinal stenosis. Particularly in patients with normal L4–5 intervertebral height, the LF and facet joints should be assessed for symmetric or asymmetric concordant disease. In patients with lumbar pain with facet joint and LF enhancement, both infection and severe degenerative disease should be kept in mind. Furthermore, in the presence of significant LF thickening and FH, gadolinium-based contrast administration could be considered to determine if the facet disease is a cause of pain generation.

In addition, facet degenerative changes and LF disease should be particularly noted in the interpreting radiologist's final report, even when the intervertebral disk spaces appear normal. This is especially important when the referring physician is considering an intervention for relief of pain and/or neurologic symptoms. Identifying “pure” LF pathology may mitigate the need for extensive spinal surgery and prompt the surgeon to undertake a minimally invasive technique.¹⁰ In addition, the rich bilevel innervation of the posterior elements by the posterior ramus of the spinal nerve can produce referred pain.⁴ With radicular distribution at the 2 adjacent ipsilateral facet levels, detailed identification of the pathologic facet and LF levels can help explain the patient's symptoms in such cases. Drug therapy with anti-inflammatory agents may help reduce or control LF thickening because it has been found to be a scarring phenomenon.¹⁵

This study had several limitations. Age and sex were not considered when stratifying patients in 1 of 3 groups because our goal was simply to assess whether LF thickening can be seen independent of DSN. The analysis of disk space heights and FH changes was subjective; the study was not prospective.

Future studies could include assessment of normal and abnormal LF thickness as it relates to age and sex and/or could assess LF enhancement in a greater number of subjects.