Neck Solutions

Intervertebral Disc: Anatomy Physiology Pathophysiology Treatment

From: Pain Practice, Volume 8, Issue 1, 2008 18–44

Back pain is strongly associated with degeneration of the intervertebral disc. Disc degeneration, although in many cases asymptomatic, is also associated with sciatica and disc herniation or prolapse. It alters disc height and the mechanics of the rest of the spinal column, possibly adversely affecting the behavior of other spinal structures such as muscles and ligaments. In the long term, it can lead to spinal stenosis, a major cause of pain and disability in the elderly; its incidence is rising exponentially with current demographic changes and an increased aged population.

The loss of proteoglycan in degenerate discs has a major effect on the disc’s load-bearing behavior. With loss of proteoglycan, the osmotic pressure of the disc falls and the disc is less able to maintain hydration under load; degenerate discs have a lower water content than do normal age-matched discs, and when loaded they lose height and fluid more rapidly: the discs tend to bulge. Loss of proteoglycan and matrix disorganization has other important mechanical effects; because of the subsequent loss of hydration, degenerated discs no longer behave hydrostatically under load. Loading may thus lead to inappropriate stress concentrations along the endplate or in the annulus; the stress concentrations seen in degenerate discs have also been associated with discogenic pain produced during discography.

Such major changes in disc behavior have a strong influence on other spinal structures, and may affect their function and predispose them to injury. For instance, as a result of the rapid loss of disc height under load in degenerate discs, apophyseal joints adjacent to such disk may be subject to abnormal loads and eventually develop osteoarthritic changes. Loss of disc height can also affect other structures. It reduces the tensional forces on the ligamentum flavum and hence may cause remodeling and thickening. With consequent loss of elasticity, the ligament will tend to bulge into the spinal canal, leading to spinal stenosis—an increasing problem as the population ages.

Loss of proteoglycans also influences the movement of molecules into and out of the disc. Aggrecan, because of its high concentration and charge in the normal disc, prevents movement of large uncharged molecules such as serum proteins and cytokines into and through the matrix. The fall in concentration of aggrecan in degeneration could thus facilitate loss of small, but osmotically active, aggrecan fragments from the disc, possibly accelerating a degenerative cascade. In addition, loss of aggrecan would allow increased penetration of large molecules such as growth factor complexes and cytokines into the disc, affecting cellular behavior and possibly the progression of degeneration. The increased vascular and neural ingrowth seen in degenerate discs and associated with chronic back pain is also probably associated with proteoglycan loss because disc aggrecan has been shown to inhibit neural ingrowth.

It is now clear that herniation-induced pressure on the nerve root cannot alone be the cause of pain because more than 70% of “normal,” asymptomatic people have disc prolapses pressurizing the nerve roots but no pain. A past and current hypothesis is that, in symptomatic individuals, the nerves are somehow sensitized to the pressure, possibly by molecules arising from an inflammatory cascade from arachidonic acid through to prostaglandin E2, thromboxane, phospholipase A2, tumor necrosis factor-a, the interleukins, and MMPs. These molecules can be produced by cells of herniated discs and because of the close physical contact between the nerve root and disc following herniation they may be able to sensitize the nerve root. The exact sequence of events and specific molecules that are involved have not been identified.

Abnormal mechanical loads are also thought to provide a pathway to disc degeneration. For many decades, it was suggested that a major cause of back problems is injury, often work-related, that causes structural damage. It is believed that such an injury initiates a pathway that leads to disc degeneration and finally to clinical symptoms and back pain. Although intense exercise does not appear to affect discs adversely and discs are reported to respond to some long-term loading regimens by increasing proteoglycan content, experimental overloading or injury to the disc can induce degenerative changes.

More recent work suggests that the factors that lead to disc degeneration may have important genetic components. Several studies have reported a strong familial predisposition for disc degeneration and herniation. Findings from two different twin studies conducted during the past decade showed heritability exceeding 60%. Magnetic resonance images in identical twins were very similar with respect to the spinal columns and the patterns of disc degeneration.

Genes associated with disc generation have been identified. Individuals with a polymorphism in the aggrecan gene were found to be at risk for early disc degeneration. Studies of transgenic mice have demonstrated that mutations in structural matrix molecules such as aggrecan, collagen II, and collagen IX can lead to disc degeneration. Mutations in genes other than those of structural matrix macromolecules have also been associated with disc degeneration.

The pain pathways for discogenic pain are still very controversial. Traditionally, pain signals that originate in the nerve roots adjacent to the disc move from that root, into the corresponding dorsal root ganglion (DRG) and into the spinal cord. However, recent new research suggests that pain signals from the lower lumbar discs (L4 and L5) are detoured up the sympathetic nerves (gray ramus communicans) and into the upper lumbar DRGs—especially at the L2 level. Clinically, in some patients it then would be possible for patients with L4 and L5 disc pathology to have L1 or L2 dermatomal pain (groin and anterior thigh pain).

This is an excellent article on the anatomy, physiology, pathophysiology and treatment of disc problems. There are many clearly illustrated diagrams and it incorporates many new technologies in the treatment section. Very nicely done and comprehensive. I highly recommend this article for anyone interested in a comprehensive view with up to date literature on disc problems.