Lower back pain is one of the most common complaints seen globally, affecting people from all ages and walks of life. Approximately 80% of the population sustains an episode once in their lifetime, and out of the many people experiencing lower back pain due to a slipped disc, approximately 95% of disc herniations in the lumbar area occur at L4-L5 or L5-S1 (1). Hence, an L5/S1 herniated disc is an incredibly common area of complaint. But why? And does age, and disc degeneration, contribute to this?
Anatomical insights – How disc degeneration/ligamentum flavum hypertrophy occurs
When people talk about disc degeneration, we are talking about the naturally occurring changes that occur in the spine. ‘Wear and tear’ is the term often heard, indicating the stresses that occur in our spine over time as we age that causes changes to the spinal structures.
Usually, it begins with small tears in the annulus (outer rings) and reduced water content in the nucleus pulposus (inner centre) of the spinal discs, osteophyte growth (overgrowth of bone from friction, like bone spurs), and then gradual narrowing of the disc spaces with some people experiencing irritation of the adjacent nerve roots (‘nerve root compression’).
The structure of disk degenerative disease
With more advanced degeneration, the facet joints around the discs and surrounding soft tissue like the ligamentum flavum may also be affected, resulting in canal narrowing also known as ‘degenerative stenosis’. Normal ligamentum flavum tissues are composed of 80% elastic fibers and 20% collagen fibers.
Upon hypertrophy due to extra mechanical stress placed on it throughout the lifetime, there is a loss of elastic fibers and an increase in collagen fibers, resulting in fibrosis, aka thickening. These histological changes are similar to tissue scarring during the post-inflammatory repair process in other organs (2). With enough thickening and ‘scarring’, it may develop enough to encroach into the spaces of the spine, causing less space for the exiting nerve roots; hence, resulting in low back pain, pain going down the leg (sciatica) and even weakness and difficulty walking.
Thickening of the ligamentum flavum causing spinal canal stenosis
How does that lead to an L5/S1 slipped disc?
As mentioned before, it doesn’t lead to a slipped disc per se, but causes spinal canal narrowing and stenosis. Posterior spinal structures, including ligamentum flavum thickness, play a major role in lumbar spinal canal stenosis occurring as it covers a considerable part of the posterior and lateral spinal canal walls.
As ligamentum flavum thickening can reduce spinal canal diameter, this ligamentum flavum hypertrophy has been considered as a cause of spinal stenosis, often causing symptoms similar to an L5/S1 herniated disc. Canal narrowing mechanically compresses the nerve root or cauda equina and contributes to lower back pain and sciatica.
Normal spine vs L5/S1 Slipped disc vs Ligamentum flavum hypertrophy
The treatment for ligamentum flavum hypertrophy focuses on a 12-week course of physiotherapy, focusing on reducing the tightness of the muscles around the back and strengthening the intrinsic muscles of the spine and core to stabilise the spinal column, strengthening the hips as well to take the load off the lower back, and movement pattern retraining to form a good foundation for your movements.
Other modalities may be involved if there is a primary symptom of pain, similar to treatments for an L5/S1 disc bulge, such as electrotherapy, EMS (electrical muscle stimulation), and lumbar traction decompression therapy using our specific machine from HillDT.
References
- Amin, R. M., Andrade, N. S., & Neuman, B. J. (2017). Lumbar Disc Herniation. Current reviews in musculoskeletal medicine, 10(4), 507–516. https://doi.org/10.1007/s12178-017-9441-4
- Yoshiiwa, T. et al. (2016). Analysis of the Relationship between Ligamentum Flavum Thickening and Lumbar Segmental Instability, Disc Degeneration, and Facet Joint Osteoarthritis in Lumbar Spinal Stenosis. Asian spine journal, 10(6), 1132–1140. https://doi.org/10.4184/asj.2016.10.6.1132