The lumbar ligamentum flavum is the thickest and most clinically significant portion of the flavum, forming the posterior spinal canal wall and resisting lumbar flexion. Its high elastic fibre content stores energy during forward bending and releases it to assist passive return to upright. Hypertrophy of the lumbar flavum is the primary cause of central spinal stenosis and neurogenic claudication in older adults, as the thickened ligament buckles into the canal in extension and compresses the cauda equina.
| Origin | Anterior surface of the superior vertebral lamina |
|---|---|
| Insertion | Posterior surface of the inferior vertebral lamina below |
| Actions | Resists lumbar flexion with stored elastic energy; forms the posterior spinal canal wall; assists passive return to upright from flexion |
|---|
Lumbar ligamentum flavum hypertrophy exceeding 4 mm is considered pathological and is the dominant cause of central spinal canal stenosis at L4-L5. The classic neurogenic claudication presentation — bilateral buttock and leg pain with walking that is relieved by sitting or lumbar flexion (shopping trolley sign) — reflects cauda equina decompression when the flavum unfolds in flexion. Flavum removal (flavectomy or laminectomy) decompresses the canal and reliably relieves neurogenic claudication in properly selected patients.
Flavum and facet hypertrophy producing central spinal stenosis with bilateral leg pain and weakness on walking relieved by sitting, managed with laminectomy or interlaminar decompression.
