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Bulging Discs and Trauma: Causality and a Risk Factor

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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 simply and common finding. Historically, many have reserved the designation of bulging disc as an explanation of non-specific back pain, thereby labeling bulging discs as a category for all disc pathology in the creation of 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 Schlegel (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 stereo photogrammetric 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.” (pg. 438-439)


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


In 2011 Fardone and Milette reported 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.” pg. E96


In 2014 Fardone, Williams, Dohring, Murtagh, Rothman and Sze reported:











The above report by Fardone et. al in 2014 differs significantly from his collaboration and reporting in 2001. The earlier report stated that a bulge is usually 50% or 180 degrees of the circumference and in 2014 reported 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.



According to Robert Peyster MD, CAQ Neuroradiology, who trained at Harvard’s Massachusetts General Hospital, is currently the Chief of Neuroradiology at the State University of New York at Stony Brook, School of Medicine and has been well published throughout his career, circumferential or diffuse disc bulges that go beyond the disc spaced are solely degeneration of the annulus and trauma cannot play a role in etiology. He describes this distinct category and reserves it for 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 sequella to trauma or displacement of the vertebra from ligamentous laxity. However, if there is no degeneration of disc, it precludes the category of a diffuse disc bulge. 


The mechanisms of disc degeneration or diffuse disc bulging that is widely accepted is articulated well be 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 the 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.” Pg. 6


Simply put, with degeneration or diffuse disc bulging and due to abnormal loading of the vertebrate, degeneration happens as sequella.



By the literature clarifying 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 researches to be able to describe what is seen in advanced imaging and allows future literature to memorialize what Dr. Peyster describes 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 above by Fardone et. Al (2014) a “non-diffuse” or a degenerative bulging disc can be secondary to ligamentous laxity and a response to aberrant loading or angular motion. These 2 imaging findings are initially diagnosed via x-ray, MRI or CT scans, but the sequella 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).  The reported:



In short, ligament laxity can be secondary to injury/trauma and cause an elongation of the ligaments that have significant negative sequella. 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 non-diffuse disc bulge secondary to trauma over time as described by Fardone et. al. above. However, prior to the disc degenerating and being called a “non-diffuse disc bulge,” it creates an asymmetrical appearance of the disc or a non-degenerative bulge and can be focal or 25% of the circumference of the disc.



As per the AMA Guides to the Evaluation of Permanent Impairment, 5th 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:



The ICD-10 code associated with ligamentous laxity that would need to be associated with a disc bulge as sequella to trauma in this scenario would need to be M24.28. In addition, according to AMA Guides to the Evaluation of Permanent Impairment, 5th Edition the whole person impairment exclusive of the disc pathology and any ensuing radiculopathic finding is 25-28%, which is significant as the authors understand the long-term degenerative sequella that occurs when connective tissue is permanently effected as is the case with laxity of ligaments. This is a s a result of the ensuing degeneration that occurs as sequella to the biomechanical homeostatic disruption.



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) according to Kadow, Sowa, Vo and Kang (2014):

“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 a loss of matrix proteins. This promotes degenerative changes…” pg. 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 of 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.” Pg. 1294


The above 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 are diffuse disc bulges that often predate trauma and can be diagnosed demonstrably with strategically positioned osteophytes that verify the pre-existing 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 balance of that victim’s life. As reported by Garcia-Cosamalon, Valle, Callavia, Garcia-Suarez, Lopez-Muniz and Vega (2010) the intervertebral disc, previously consider aneural (lacking nerve supply), is innervated by the sinuvertebral (now known as the recurrent meningeal) nerve and supplies the outer 1/3 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, Cole, Breakwell, Michael, Chiverton, Creemers, Cross and LeMaitre (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):



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






Clinically, doctors have been experiencing diffuse disc bulge patients in an asymptomatic state reporting 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 sequella 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 feeds the central nervous system. Many of these patients clinically have to be managed by pain management physicians 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 visualize a diffuse disc bulge that has predated the trauma.  


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



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







  1. Wenger K., Schleger J., (1997) Annular bulge contours from an axial photometric method, Clinical Biomechanics 12 (7/8) pgs. 438-444
    2. Freeman A., (2009) The Cellular pathobiology of the degenerate intervertebral disc and discogenic back pain, Rheumatology 48: 5-10
    3. 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:
    4. 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
  3. Cocchiarella L., Anderson G., (2001) Guides to the Evaluation of Permanent Impairment, 5th Edition, Chicago IL, AMA Press
  4. 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
    1. José García-Cosamalón, Miguel E. Del Valle, Marta G. Calavia, Olivia García-Suárez, Alfonso López-Muñiz, Jesús Otero, José A. Vega (July 2010) Intervertebral disc, sensory nerves and neurotrophins: who is who in discogenic pain? Journal of Anatomy, Volume 217, Issue 1, pgs. 1-15,
  5. Binch A., Cole A., Breakwell L., Michael A., Chiverton N., Creemers L., Cross A. and LeMaitre C. (2015) Nerves are more abundant that blood vessels in the degenerate human intervertebral disc, Arthritis Research & Therapy, 17370, pgs. 1-10



Dr. Bill Owens is presently in private practice in Buffalo and Rochester NY and generates the majority of his new patient referrals directly from the primary care medical community.  He is an Associate Adjunct Professor at the State University of New York at Buffalo School of Medicine and Biomedical Sciences as well as the University of Bridgeport, College of Chiropractic and an Adjunct Professor of Clinical Sciences at Texas Chiropractic College.  He also works directly with doctors of chiropractic to help them build relationships with medical providers in their community. He can be reached at or or 716-228-3847  

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