Academy of Chiropractic’s

Lawyers PI Program


 From the Desk of:



*Not recognized by the Florida State Board of Chiropractic Medicine

"Bulging Discs and Pain From Trauma and Non-Trauma Cases"

The graphic to the left represents the spinal cord and nerves. The recurrent meningeal nerve is highlighted. It was formerly called the "sinuvertebral nerve" and innervates the outer 1/3 of the annular fibers. This explains why when there is an interruption of the disc, either a bulge (degeneration), a herniation (tear), or an annular tear, pain is involved. The fibers that are involved are the C-Fibers as explained in the abstract below.

The recurrent meningeal nerve explains why, in the absence of cord or root compression, the patient can experience pain as the C-fibers in the outer 1/3 of the annulus get irritated and are part of the inflammatory and pain process. This easily explains herniations and annular tear pain and inflammation, but the following new research, first published in July, 2010, explains pain from bulging discs and we will go one step further and explain the mechanism when trauma is introduced into a bulged disc. 


García-Cosamalón, J.,  del Valle, M. E.,  Calavia, M. G., García-Suárez, O., López-Muñiz, A., Otero, J., & Vega, J. A. (2010). Intervertebral disc, sensory nerves and neurotrophins: Who is who in discogenic pain? Journal of Anatomy, 217(1), 1-15


"The normal intervertebral disc (IVD) is a poorly innervated organ supplied only by sensory (mainly nociceptive) and postganglionic sympathetic (vasomotor efferents) nerve fibers. Interestingly, upon degeneration, the IVD becomes densely innervated even in regions that in normal conditions lack innervation. This increased innervation has been associated with pain of IVD origin. The mechanisms responsible for nerve growth and hyperinnervation of pathological IVDs have not been fully elucidated. Among the molecules that are presumably involved in this process are some members of the family of neurotrophins (NTs), which are known to have both neurotrophic and neurotropic properties and regulate the density and distribution of nerve fibers in peripheral tissues. NTs and their receptors are expressed in healthy IVDs but much higher levels have been observed in pathological IVDs, thus suggesting a correlation between levels of expression of NTs and density of innervation in IVDs. In addition, NTs also play a role in inflammatory responses and pain transmission (C-Fibers) by increasing the expression of pain-related peptides and modulating synapses of nociceptive neurons at the spinal cord. This article reviews current knowledge about the innervation of IVDs, NTs and NT receptors, expression of NTs and their receptors in IVDs as well as in the sensory neurons innervating the IVDs, the proinflammatory role of NTs, NTs as nociception regulators, and the potential network of discogenic pain involving NTs" ( García-Cosamalón et al., 2010, p. 1).

The above abstract is from an article that explains how when there is a disc bulge or degeneration, the resident C-fibers (nerves) in the annulus go through the process of "ingrowth" and further invaginate the annulus and in some cases, the nucleus, of the disc. This results in the disc being susceptible to generating more pain impulses as more of the disc is now innervated. In reality, the disc is thinning which is the end result of degeneration, but the nerve fibers do not thin with the annulus, leaving the resident nerves new places to go. The following graph taken from the above citation illuminates the process.


The top picture shows a healthy disc, while the bottom picture, although not graphically proportionate, represents a thinned, degenerated disc. You can see how the authors illustrated the "ingrowth" of the nerves.

When there is subsequent trauma to a previously degenerated disc, this becomes a risk factor. The risk factor is that if it was a healthy disc, the disc would have a greater amount of structural integrity and the neurological innervation wouldn't be as invasive. During the trauma process, a bulged disc, due to its decreased structural integrity, will be subject to greater deformation and expose the victim to greater pain and inflammation as a result of the disc becoming more easily deformed. Also, as a "new" nerve ending (nerve bud) grows, it releases factors to assist the process of forming additional links to other nerve endings. This process actually helps make more nerve fiber endings, which in the case of pain fibers, actually makes the body better able to carry pain signals to the brain. More input to the brain makes it better and better at receiving pain signals, thereby causing you to feel "more" pain. The reality is that the nerve pathways for pain are now much more efficient at sending signals and may need even less stimuli to do so (so it takes less "stimulus" to actually even fire it off).

Additionally, when a nerve is damaged, it tries to survive by firing off signals without stimulation which we see on EMG as spontaneous potentials. In the event that these nerves reconnect with other nerves, they tend to do so in higher numbers, thereby showing us on EMG large MUPs (motor unit action potentials).

This answers many clinical questions that have arisen for far too long as to why the patient, in the absence of a new herniation or other pathology, is now experiencing significantly more pain with the only clinical finding being a previously degenerated disc. We will not know the exact causes until our diagnostic imaging reaches a much higher level of clarity at the disc level.