Pathophysiology

Two of the most common pain generators in the lumbar spine are 1) the disc, and 2) the facet joints. Typically, the disc bears more weight in all positions, but increases to around 90% of forces transmitted through the lumbar spine in SITTING. Rotation and lifting, when added to lumbar flexion (bending at the waist), naturally will increase the forces on the disc. As the degenerative process progresses, the disc-facets force transmission approaches parity; with facet mediated pain being more common the older you get, and discogenic pain being more common overall. However, this is a generalization.

Persistent, recurrent, and/or excessive forces to the spine lead to microtrauma of the disc and facet joints, triggering and continuing the degenerative process. The degenerative cascade, described by Kirkaldy-Willis, is the widely accepted pathophysiologic model describing the degenerative process as it affects the lumbar spine and individual motion segments.

The best analogy that I routinely use for the disc is a jelly donut. There is the nucleus (jelly) that is mostly water-based, and then the tough outer collagen fibers called the annulus (the outer part of the jelly donut). The degeneration is initially characterized histologically by tears or fissures in the outer annulus. Tears can interrupt blood supply to the disc and impair nutritional supply and waste removal. Since the outer one third of the annular wall is innervated (has nerve endings, ie pain receptors), tears or fissures in this area may be painful. Strong experimental evidence suggests that most episodes of low back pain are a consequence of disc injury, rather than muscle/tendon/ligament strain.

Changes in the composition of the collagen result in diminished capacity for imbibing water, causing loss of nuclear pressure and leading to pressure on the annulus.

MRI at this stage may reveal desiccation (dehydration, or a “dark disc”), disk bulging, or a “high-intensity zone (HIZ)” or tear in the annulus. Structural changes of the facet joint following disc degeneration is acknowledged widely, but this doesn’t always follow disc degeneration. Changes associated with the facet joints during this degeneration may include inflammation and hypomobility. The facet joint may serve as a pain generator, as described earlier.

Multiple syndromes follow this degeneration. With facet arthritis, that segment can become unstable, and one vertebral body can “slip” forward on another. This is called spondylolisthesis. Weak discs can bulge or protrude or herniate out into the canal and not only cause back pain (from the pain receptors on the disc, but also impinge on the nerves that are traveling in the canal just behind the disc. These nerves (commonly called the sciatic nerve) are the ones that control sensation in the legs and muscles in the legs, as well as bowel and bladder function. Also, the less padding (discs) there is between the bones, the more bones spurs form (spondylosis), which can also obstruct the holes (foramen) that the lower extremity nerves are traveling through.

by Nathan S. Walters, MD

Ref: R. Patel, MD, C. Slipman, MD, Lumbar Degenerative Disk Disease
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