Bulging Discs and Trauma: Causality and a Risk Factor

The effects of Chiropractic Spinal Manipulation on Urinary Incontinence in patients with Low Back Pain and Radiculopathy: a retrospective case-series report  
September 25, 2017

Bulging Discs and Trauma: Causality and a Risk Factor



William J. Owens DC, DAAMLP

Bulging discs historically have been called bulges, ruptures, collapsed, pinched nerves, protrusions, slipped discs, prolapsed discs, and a myriad of other names to describe what is a very simple and common finding. In the past, many have reserved the designation of “bulging disc” as an explanation of nonspecific back pain, thereby labeling bulging discs as category for all disc pathology when creating a plausible diagnosis in the absence of a concrete diagnosis or a full understanding of contemporary nomenclature.

To illuminate the confusion through the years, Wenger and Schleger (1997) reported that:

Previous in vitro studies of annular bulge have produced widely varying results, reflecting fundamentally different test methods and regions of interest. Brown et al. first demonstrated with dial gauges that bulges under bending load increase on the concave side. This was confirmed in a modern, similar study by Reuber et al. who furthermore concluded that bulge was greater laterally than posterolateral. Brinckmann and Horst introduced a rotating probe technique, which allowed the bulge to be measured in fine increments around the periphery of the disc. Conversely to other findings, they reported a fairly uniform bulge contour in the typical intact specimen. Lin et al. found anterior bulge to be slightly greater than lateral bulge by using a dial gauge technique, and Stokes, using a streophotogrammetric technique, found anterior bulge to be twice that of posterolateral bulge. Shahs, on the other hand, found with dial gauges that the greatest bulge was posterolateral. (p. 438-439)

Those researchers were reporting studies performed in the 1970s and 1980s that set the foundation for much confusion that still persists at many levels. With the advents of MRI and ensuing imaging technological advances that further visualized the morphology and pathology of the disc, Fardon and Milette (2001) reported one of the first concise explanations of disc pathology that has been widely accepted by the radiologic community.

In 2011, Fardon and Milette reported the following regarding bulging discs:

Symmetrical presence (or apparent presence) of disc tissue “circumferentially”

(50-100%) beyond the edges of the ring apophyses may be described as a “bulging disc” or “bulging appearance” and is not considered a form of herniation. Furthermore, “bulging” is a descriptive term for the shape of the disc contour and not a diagnostic category. (p. E96)

In 2014, Fardon et al. reported:

Degeneration may include any or all of the following: desiccation, fibrosis, narrowing of the disc space, diffuse bulging of the annulus beyond the disc space, fissuring (i.e., annular fissures), mucinous degeneration of the annulus, intradiscal gas, osteophytes of the vertebral apophyses, defects, inflammatory changes, and the sclerosis of the endplates. (p. 2528)

Bulging disc, bulge (noun [n]), bulge (verb [v])

  1. A disc in which the contour of the outer annulus extends, or appears to extend, in the horizontal (axial) plane beyond the edges of the disc space, usually greater than 25% (90°) of the circumference of the disc and usually less than 3mm beyond the edges of the vertebral body apophysis.
  2. (Nonstandard) A disc in which the outer margin extends over a broad base beyond the edges of the disc space.
  3. (Nonstandard) Mild, diffuse, smooth displacement of disc.
  4. (Nonstandard) Any disc displacement at the discal level.

Note: Bulging is an observation of the contour of the outer disc and is not a specific diagnosis. Bulging has been variously ascribed to redundancy of the annulus, secondary to the loss of disc space height, ligamentous laxity, response to loading or angular motion, remodeling in response to adjacent pathology, unrecognized and atypical herniation, and illusion from volume averaging on CT axial images. Mild, symmetric, posterior disc bulging may be normal finding at L5-S1. Bulging may or may not represent pathological change, physiological variant, or normalcy. Bulging is not a form of herniation; discs known to be herniation should be diagnosed as herniation or, when appropriate, as specific types of herniation. (p. 2537)

That report by Fardon et al. in 2014 differs significantly from his collaboration and reporting in 2001. The earlier report stated that a herniation is usually 50% or 180 degrees of the circumference, and the 2014 report stated that it is now greater than 25%or 90 degrees. This designation now allows many lesions to be more definitively classified when the nucleus appears intact with no herniation possible and a smaller circumference involved.

Robert Peyster, MD, CAQ Neuroradiology has been well published throughout his career, trained at Harvard’s Massachusetts General Hospital, and is currently the chief of neuroradiology at the State University of New York at Stony Brook, School of Medicine. According to him, circumferential or diffuse disc bulges that go beyond the disc space are solely degeneration of the annulus and trauma cannot play a role in etiology. He describes this distinct category and reserves it only for circumferential extensions beyond the endplate in agreement with today’s literature. However, he further defines a previously poorly defined category, the directional displacement with no annulus degeneration and terms that a “pseudo-protrusion” that can be as sequela to trauma or displacement of the vertebra from ligamentous laxity. However, if there is no degeneration of the disc, it precludes the category of a diffuse disc bulge.

The mechanisms of disc degeneration or diffuse disc bulging that are widely accepted are articulated well by Freeman (2008):

The tissue changes of degeneration are increased breakdown of matrix, altered matrix synthesis (consisting largely of a change from type II to type I collagen synthesis and decreased synthesis of aggrecan), cell loss through apoptosis and in situ replication of surviving cells to form clusters. The process extends to the annulus fibrosis largely as a result of altered loading consequent upon reduced separation between vertebrae (“loss of disc height”) as the amount of aggrecan and swelling pressure of the nucleus pulposis fall. In this setting, the normal balance between forces generated in the nucleus pulposis and annulus fibrosis is lost, resulting in decreased tension in the collagen fibers in the annulus fibrosis, which promotes shock loading. (p.6)

Simply put, with degeneration or diffuse disc bulging and abnormal loading of the vertebrae, degeneration happens as sequellae.

Since the literature clarifies the designation of bulging discs as an observation of the contour of the disc and not a “hard definitive category,” it allows consensus between both practitioners and researchers to be able to describe what is seen in advanced imaging, and it allows future literature to memorialize what Dr. Peyster described as a “pseudo-protrusion.” Until then, based upon current standards, a disc bulge that is not diffuse can have etiology in trauma and give practitioners a more complete understanding of disc morphology/pathology with respect to causality in constructing an accurate diagnosis, prognosis, and treatment plan.

As previously described by Fardon et al. (2014), a “non-diffuse” or a degenerative bulging disc can be secondary to ligamentous laxity and response to aberrant loading or angular motion. These two imaging findings are initially diagnosed via X-ray, MRI, or CT scans, but the sequel of the disc morphology/pathology is best visualized via MRI that either meets or exceeds the slice thickness guidelines by the American College of Radiology.

When considering laxity of ligaments, the ligaments become elongated, which causes excessive movement and is in response to injury, as reported by Steilen, Hauser, Woldin, and Sawyer (2014). They reported:

…this can cause a number of other symptoms including, but not limited to, nerve irritation and vertebrobasilar insufficiency with associated vertigo, tinnitus, dizziness, facial pain, arm pain, and migraine headaches. In the lower cervical spine (C3-C7), this can cause muscle spasms, crepitation, and/or paresthesia in addition to chronic neck pain. In either case, the presence of excessive motion between two adjacent cervical vertebrae and these associated symptoms is described as cervical instability. (p.326)

In short, ligament laxity can be secondary to injury/trauma and can cause elongation of the ligaments that have significant negative sequela. However, when the ligaments become lax, this in turn creates a hypermobility of adjacent vertebral joints and results in abnormal loading and/or angular motion (formally termed AOMSI, or alteration of motion segment integrity) and then becomes the causal factor of the nondiffuse disc bulge secondary to trauma over time, as described by Fardon et al. earlier. However, prior to the disc degenerating and being called a “nondiffuse disc bulge,” it creates an asymmetrical appearance of the disc or a nondegenerative bulge and can be focal or 25% of the circumference of the disc.

As per the AMA guidelines to the Evaluation of Permanent Impairment (fifth edition), to determine if there is ligamentous laxity that can be the competent producing cause of alteration of motion segment instability you need to consider the following:

Motion of the individual spine segments cannot be determined by a physical examination but is evaluated with flexion and extension roetgenograms. Loss of motion segment integrity is defined as an anteroposterior motion of one vertebrae over another that is greater than 3.5 mm in the cervical spine, greater than 2.5 mm in the thoracic spine and greater than 4.5 mm in the lumbar spine. In the cervical spine, loss of motion segment integrity is defined as motion at the level in question that is more than 11 degrees greater than at any other adjacent level…In the lumbar spine between L1-L4 it is 15 degrees, L4-L5, 20 degrees and L5-S1, 25 degrees for alteration of motion segment integrity (verifying ligamentous laxity). (Cocchiarella and Anderson, p. 378-379).

The ICD-10 code associated with ligamentous laxity that would need to be associated with a disc bulge as sequel to trauma in this scenario would need to be M24.28. In addition, according to the AMA Guides to the Evaluation of Permanent Impairment (fifth edition), the whole person impairment exclusive of the disc pathology and any ensuing radiculopathic finding is 25 to 28%, which is significant because the authors understand the long-term degenerative sequel that occurs when connective tissue is permanently affected, as is the case with laxity of ligaments. This is a result of the ensuing degeneration that occurs as sequel to the biomechanical homeostatic disruption.

According to Kadow, Sowa, Vo, and Kang (2014), once the biomechanical failure occurs that is a result of a myriad of etiologies inclusive of obesity, sports injuries, auto accidents, or any other traumatic event causing damage to the connective tissue (ligaments damage commonly known as sprains):

A healthy disc requires maintenance of a homeostatic environment, and when disrupted, a catabolic cascade of events occurs on a molecular level resulting in upregulation of pro-inflammatory cytokines, increased degradative enzymes, and loss of matrix proteins. This promotes degenerative changes… (p. 1903)

To further explain the phenomena, Wang and Samartzis (2014) reported that:

With disc degeneration, the increasingly lost nucleus pulposis proteoglycans leads to reduced hydrodynamic transfer or axial stresses to the outer annulus fibrosis. Concurrently, the integrity of the annulus fibrosis is despoiled with radial fissures. The endplates undergo an ossification process and further reduce the nutritional supply to the disc. (p. 1294).

That is the biochemical mechanism that occurs with abnormal biomechanics and is an insidious process that will not end until there is ankyloses or buttressing of the segments. This is also known as advanced or “end-stage spondylosis” (osteoarthritis of the spine).

The next scenario is diffuse disc bulges that often predate trauma and can be diagnosed demonstrably with strategically positioned osteophytes that verify the preexisting disc degeneration. However, the morphology (anatomy) of the degenerated or diffuse disc bulge explains the chronic pain the trauma victim experiences that can persist for the rest of that victim’s life. As reported by Garcia-Cosamalon et al. (2010), the intervertebral disc, previously considered aneural (lacking nerve supply), is innervated by the sinuvertebral (now known as recurrent meningeal) nerve and supplies the outer one third of the annulus. This anatomical fact is widely held in the research community as verified via microscopic inspection.

However, it was reported by both Garcia-Cosamalon et al. (2010) and Binch et al. (2015) that when there is degeneration of the intervertebral disc, there is an ingrowth of nerves further into the annulus and the nucleus to innervate previously aneural regions. It was reported by Garcia-Cosamalon et al. (2010):

In these conditions, the density of mechanoreceptors in the superficial layers of IVDs is increased. Dorsal root ganglia (DRGs) contain different types of sensory neurons that project to the IVD and to the dorsal horn of the spinal cord (DH of SC). Thin myelinated Aδ fibers and unmyelinated C fibers arise from small neurons, which in the spinal cord, synapse in lamina I and II and mediate nociception. The myelinated Aβ fibers arise from intermediate neurons; at the periphery they form slowly and rapidly adapting low-threshold mechanoreceptors, and synapse in lamina III and IV in the dorsal horn of the spinal cord; they mediate sensations of touch, pressure, and vibration. Most of the sensory nerve fibers innervating the IVD are Aδ or C fibers. (p. 4).

This means that the density of nerves increases and the entire structure becomes more sensitive with “low threshold” nerves that communicate directly with the central nervous system. In short, the preexisting diffuse disc bulge then becomes a “risk factor” for negative sequel that ordinarily would not be experienced if the disc was healthy prior to the trauma.

Note: A risk factor is something that increases the risk to get a disease or make something worse that ordinarily wouldn’t be problematic. In this scenario, it is the textbook definition of a risk factor causing a worse problem.

Clinically, doctors have been experiencing diffuse disc bulge patients in an asymptomatic state who report significant persistent pain, sometimes for a lifetime, as a result of the discs being traumatized in a discal environment that is now more innervated (nerves) and has a lower threshold of pain. As sequela to trauma, a pain process initiates that can continually be exacerbated by something as simple as moving because you now have more nerves with lower threshold of sensory input (pain) that feed the central nervous system. Many of these patients clinically have to be managed by pain management physicians and often with injections and/or oral analgesics that can persist because conservative care can increase the amount of irritation. The demonstrative evidence to conclude an accurate diagnosis is an MRI and to visualize a diffuse disc bulge that has predated the trauma.

In addition to the previously mentioned generalized or radicular pain caused by now what can be considered an aggravation of a preexisting problem, we can further causally relate the trauma with the presence or the absence of radicular symptomatology. Del Grande, Maus, and Carrino (2012) reported:

Only a close concordance, a key in lock fit, of an imaging finding and an individual patient’s pain syndrome can suggest causation, which further implies that the imager must know the nature of a radicular pain syndrome if he/she is to suggest a causal lesion. Close communication between clinician and imager via the medical record, an intake document at the imaging site detailing the pain syndrome, or direct patient interview by the imager is necessary. (p. 640)

Simply put, if there is no radicular pain before the trauma and there is pain afterward, then the pain is causally related.


There are now, based upon the literature and well-respected experts, categories of disc bulges that can be deemed as direct sequela from trauma versus those cases where there is preexisting degeneration. It also can now be concluded, again based upon the literature, that those patients can have an aggravation of the preexisting condition that could persist for a lifetime and require perpetual care. To conclude these findings, a doctor trained in understanding the underlying pathology and sequela must be consulted to be able to render an accurate diagnosis that is demonstrable.



Wenger, K., & Schleger, J. (1997). Annular bulge contours from an axial photometric method. Clinical biomechanics, 12(7/8), 438-444.
Fardon, D.F., & Milette, P.C. (2001). Nomenclature and classification of lumbar disc pathology. Recommendations of the combined task forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine, 26(5), E93-E113.
Fardon, D.F., Williams, A. L., Dohring, E. J., Murtagh, F. R., Gabriel Rothman, S. L., & Sze, G. K. (2014). Lumbar disc nomenclature: Version 2.0. Recommendations of the combined task forces of the North American Spine Society. American Society of Spine Radiology, and American Society of Neuroradiology. Spine, 39(24), 2525-2545.
Freeman A. (2009). The cellular pathobiology of the degenerate intervertebral disc and discogenic back pain. Rheumatology, 48, 5-10.
American College of Radiology (2014) ACR-ASNR-SCBT-MR practice parameter for the performance of magnetic resonance imaging (MRI) of the adult spine. Retrieved from: http://www.acr.org/~/media/ACR/Documents/ PGTS/guidelines/MRI_Adult_Spine.pdf
Steilen, D., Hauser, R., Woldin, B., & Sawyer S. (2014) Chronic neck pain: Making the connection between capsular ligament laxity and cervical instability. Open Orthopedic Journal, 8, 326-345.
Cocciarella L., &Anderson, G. (2001). Guides to the Evaluation of Permanent Impairment, Fifth Edition. Chicago, IL: AMA Press.
Kadow, T., Sowa, G., Vo, N., & Kang, J. (2014). Molecular basis of intervertebral disc degeneration and herniations: What are the important translational questions. Clinical Orthopaedics and Related Research, 473, 1903-1912.
Garcia-Cosamalon, J., Del Valle, M.E., Calavia, M.G., Garcia-Suarez, O., Lopez-Muniz, 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.
Binch, A., Cole, A., Breakwell, L., Michael, A., Chiverton, N., Creemers, L., Cross, A., & LeMaitre, C. (2015). Nerves are more abundant than blood vessels in the degenerate human intervertebral disc. Arthritis Research and Therapy, 17370, 1-10.

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