Age Dating Disc Injury:

Herniations and Bulges

Causally Relating Traumatic Disc

By:  Studin, M., Peyster R., Owens W., Sundby P.  (2016) 

CITATION: Studin M., Owens W., Peyster R., Sundby P. (2016) Age Dating Disc Injuries, Causally Relating Traumatic Disc, American Chiropractor, 34 (8) 38, 40-44

When considering disc pathology, one of the most asked questions is, “How do you determine causality and age-date the lesion?” The medical literature has purposefully avoided answering this type of question to apparently avoid any appearance of pandering to the medical-legal community. Fardone and Milette (2001) reported, “The term herniated disc does not infer knowledge of cause, relation to injury or activity, concordance with symptoms, or need for treatment” (p. E108).

14 years later, upon further evidence, Fardon et al. (2014) reported:

The category of trauma includes disruption of the disc associated with physical and/or imaging evidence of violent fracture and/or dislocation and does not include repetitive injury, contribution of less than violent trauma to the degenerative process, fragmentation of the ring apophysis in conjunction with disc herniation, or disc abnormalities in association with degenerative subluxations. Whether or not a ‘less than violent’ injury has contributed to or been superimposed on a degenerative change is a clinical judgment that cannot be made on the basis of images alone; therefore, from the standpoint of description of images, such discs, in the absence of significant imaging evidence of associated violent injury, should be classified as degeneration rather than trauma. (p. 2531)

As described by Fardone above, the definition and understanding of “violent injury” becomes an important arbiter in determining causality and lends an important understanding to age-date the herniation and/or bulge. In understanding the nature of Fardone’s tag of “violent,” science gives us answers rather than intuitive perceptions or rhetoric and the quantification of energy transferences to victim in accidents gives us those answers. The rate of change in speed (ΔV) of any free moving body is what contributes to quantifying energy transfer and can be directly correlated to injury. Brault, Wheeler, Siegmund, and Brault (1998) reported that in rear-end collision testing, it was determined whiplash could occur with a change in speed as low as 2.49 mph ΔV where there was no visual damage to the automobile. 

Krafft et al (2002) reported symptoms at a ΔV of 12.5 km (7.77 mph) and an injury mean threshold of 4.2 g’s for males and a ΔV of 9.6 km (5.97 mph) with a mean of 3.6 g’s for females.  Using this data, a corresponding window of time can be calculated between .084 seconds for males and .080 seconds for females (verifying that females are more at risk than males), resulting in a mean of .082 seconds. As evidenced above, acceleration (ΔV) is important as it is part of the physics to determine g forces that explains injury thresholds and gives a numerical value to Fardone et al.’s (2014) use of the descriptor “violent injury.” 

The risk for injury is present in a vehicle no matter the initial speeds or damage to the protective equipment as transference of forces is the prime factor in accidents. Additionally, low speed collisions have a history of little to no damage; therefore, little or no energy is absorbed by the safety equipment & design of the vehicles, yet the occupant is subject to these forces even with safety restraints.  Because of these factors only a few pieces of information are needed to quantify the energy transfer an occupant is subjected to. 

1. Speed – just before the collision of each vehicle involved.
2. Weight of each vehicle and its occupants.
3. Time (t) of .082 seconds

Two examples:

Example A: A 6,100-pound SUV traveling at 7 mph rear ends a 4,200-pound car stopped at a red light, the SUV stops as a result of the collision.  The car (and its occupants) will experience a resultant ΔV of 10.67 mph (not to be confused with the speed of the bullet vehicle that struck the target vehicle). 

Example B: A 30,000-pound truck and trailer backing up at 2 mph backs into rear of a 4,800-pound occupied parked van, the truck stops as a result of the collision.  The van (and its occupants) will experience a ΔV of 12.5 mph.

Regarding Krafft et al (2002)’s Tables 1-4 (Pg. 3):  In the both examples above, the acceleration threshold for injury of males and females were exceeded. Both collisions would be traditionally classified as low speed with potentially no deformity of the vehicles. Just to underscore the injury potential at low speeds, the second example occurred at 2 mph where the physics of the crash offered demonstrable evidence of threshold forces sufficient to cause bodily injury.

Because Fardone et al (2014) uses the word “violent” with no qualifying parameters, the above examples offer insight through science on how transferred forces impact the human body with a predictable threshold for injury. Since the word “violent” is a subjective descriptor, one must utilize science and not consider generalities as illustrated by the low speed examples above.

Del Grande, Maus and Carrino (2012) reported that although there were varying reports of asymptomatic herniations in the literature, only a post-traumatic finding of radicular, or nerve root, pain can be definitive for determining causality.

Del Grande, Maus and Carrino (2012) wrote:

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).

Therefore, it is critical to ensure that patients have a complete history taken and an examination performed by a credentialed health care provider that is trained in trauma care. Many practitioners are licensed to treat the trauma case, but many are ill equipped in training and experience to ensure an accurate diagnosis and determine proper relationship to causality.

Beyond radiating symptomatology, although as Del Grande, Maus and Carrino (2012) have reported as an accepted parameter for determining herniation causality, it is important to realize that radiating clinical symptoms arising out of injury to an intervertebral disc are dependent on the anatomical positioning of the injured and inflamed disc material.  It is only when the disc herniation is of a lateralized nature that the segmental nerve root is compressed or inflamed producing radiation of axial symptoms to the corresponding upper or lower extremity.  To discuss radiation as a primary indicator of acute traumatic injury to the intervertebral disc omits central disc herniations which in and of themselves do not typically produce extremity symptomology.  When it comes to acute injury in the absence of radiating symptoms, local symptomatology should also be considered in approaching a mechanism and timing of the injury.  Furthermore, one must also look at the morphology or architecture of the individual vertebrae as demonstrative evidence to age-date disc pathology inclusive of both herniations and traumatically induced directional, non-diffuse bulges as described by Fardon et al (2014).

Wolf’s Law as described by Isaacson and Bloebaum (2010), “Physical forces exerted on a bone, alter bone architecture and is a well-established principle…” (p. 1271). This has been understood and accepted as a general principle since the late 1800’s and has been verified through the past century’s research inclusive of contemporary research. Simply put, if a bone has abnormal stresses, it will change morphology or shape within expected parameters. Since these changes are “expected,” the question becomes, “How does Wolf’s Law apply to traumatic external forces and acute disc injury and how does this relate to causality?”

In order to fully understand the process, it is critical to understand the biochemical reaction (functional adaptation) that occurs with abnormal stresses on bone, which centers on bioelectric changes that occur at the cellular level. According to Issacson and Bloebaum (2010), when tissue is damaged, the injury potential creates steady local electric fields that result from ion flux (positive and negative charges moving through local cellar membranes) which is an integral part in the regeneration/remodeling of bony tissue. Bone remodeling is a tightly coupled functional system and is strongly influenced by age, activity level and mechanical loading. This functional adaptation of bone demonstrates the unique ability of bone to alter its trabecular (structural bone tissue) orientation as a result of loading conditions. According to Frost (1994), bone remodeling is a direct response to mechanical influences and strains on the osseous system. This can occur as a normal process to strengthen bone or as a response to altered anatomy, biomechanics or direct traumatic injury.  Since this is a predicable scenario, we can identify specific factors that will help us to determine whether the response was present over time or is at the beginning phase of remodeling.  That is the fundamental basis for putting a causally related date to the injury.

Isaacson and Bloebaum (2010) note that in regard to the remodeling of bone, the successful growth of additional supporting bone results from a combination of competent mechanical strain stimuli and endogenous electrical currents (bio-electrical changes). Simply put, it is the mechanical stresses and the flow of the bioelectric compounds that work in conjunction with one another to strengthen or produce additional bone to functionally “buttress” the joint segment.   The above mentioned endogenous electrical current/bioelectrical changes are more commonly known as the piezoelectricity or the body’s electrical reaction to pressure or mechanical stress. It is this electrically and mechanical-based system that subsequently controls osteogenic (osteo = bone, genic = to create) activity. The amplitude or amount of electrical potential is dependent upon on the magnitude of the mechanical bone loading, while polarity (application of the bioelectric charge) was determined by the direction of the deformed bone. Isaacson and Bloebaum (2010) reported, “The specific loading pattern of bone has been documented as an important piezoelectric parameter since potential differences in bone have been known to be caused by charge displacement during the deformation period” (p. 1271). What this means is that application of Wolf’s Law to a bony segment is dependent on the amount of mechanical stresses as well as the direction of those forces, and is therefore based on basic engineering principles in the body. The extent and direction of the bone’s response to these forces is predictable and expected. 

Additionally, Isaacson and Bloebaum (2010) noted that increased pressure surround the bone inhibits specific hormones preventing the uptake of calcium in the blood which, in turn, results in the additional uptake of calcium within bone itself, causing additional bone to be produced.  Now that we understand what is happening from a physiological perspective when the bone responds to normal or abnormal mechanical stresses, the aging processes or an acute traumatic injury, the question becomes, “Can we objectively predict this process in the human spine?”

He and Xinghua (2006) studied the predictability of bone remodeling which included both the external shape and internal bone density distribution. They extended the simulation of the external shape of bones to determine and to predict pathological changes in bone, specifically the osteophyte on the edge of a bone structure. They reported, “The significance of this work were: (1) it confirmed that osteophyte formation was an adaptive process in response to the change of mechanical environment, which can be simulated numerically by combining quantitative bone remodeling theory with finite element method. And (2) it can help to better understand the relationship between bone morphological abnormity and the mechanical environment” (He and Xinghua, 2006, p. 96).

He and Xinghua (2006) also reported that with load bearing bones such as the femur and vertebrae, mechanical factors are crucial to the morphology and changes in boney structures which relate closely to changes in mechanical environments. In addition, changes in bone structure morphology are slowly progressing processes unless other factors such as trauma or inflammation are included, at which time the processes will be accelerated to change the bone structural morphology.  What that means is that there is a “genetic timing” to the remodeling process that can be altered (increased) by the presence of specific conditions such as an acute injury or inflammation. 

According to He and Xinghua (2006), when only the local mechanical environment changes or a directional change in force coefficients is present, then only part of the vertebrae will remodel leaving the rest of the vertebrate unchanged. Simply put, if there is a one-sided lesion creating pressure unilaterally, then only that side of the disc will create an osteophyte. This is very similar to the formation of a callus on your hand or foot. “In this paper, the main pathology of osteophyte formation was associated with the structural deterioration of intervertebral disc” (He and Xinghua, 2006, p. 97).

These researchers further discuss that the remodeling process will continue until the biomechanical failure is resolved and the body has reached a biomechanical equilibrium by placing an osteophyte on the edge of the vertebrae, one whose size and strength is based upon the influencing mechanical imbalance. They concluded that only the bone in the area of mechanical imbalance would be compromised.

Although individuals have different formation rates and the osteophytes may vary in size, everyone is subject to morphological changes depending upon mechanical imbalances in the spine. He and Xinghua (2006) concluded that, “…it will actually take about more than half a year to observe the bone morphological changes…” (p. 101). This indicates that it takes approximately 6 months for an osteophyte to be demonstrable post-mechanical failure or imbalance. This again gives a time frame to better understand if pathology of the intervertebral disc has been present for a long period of time (pre-existing) or has been produced as the direct result of the specific traumatic event by lack of the existence of an osteophyte, meaning the disc pathology is less than 6 months in duration. 

In conclusion, we would like to remind the reader that, by definition, a disc is a ligament, connecting a bone to a bone and it has the structural responsibility to the vertebrate above and below to keep the spinal system in equilibrium. Damage to the disc through a tear (herniation or annular fissure) or a directional, non-diffuse bulge will create abnormal load bearing or biomechanical failure on the side of the disc lesion. Since we have previously defined the term “violent trauma” as not being dependent upon the amount of damage done to those structures either around or containing the victim and have determined there were ample force coefficients to produce injury to the spine, then based upon the current literature, we can now accurately predict in a demonstrable manner the timing of causality of the disc lesion. This is both based upon the symptomatology of the patient and/or the morphology of the vertebral structure and is a subject that can no longer be based upon rhetoric.

References:

1. 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.
2. Fardon, D. F., Williams, A. L., Dohring, E. J., Murtagh, F. R., Rothman, S. L. G., & 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, 14(11), 2525-2545.
3. Brault J. R., Wheeler J. B., Siegmund, G. P., & Brault, E. J. (1998). Clinical response of human subjects to rear-end automobile collisions. Archives of Physical Medicine and Rehabilitation, 79(1), 72-80.
4. Krafft, M., Kullgren, A., Malm, S., and Ydenius, A. (2002). Influence of crash severity on various whiplash injury symptoms: A study based on real life rear end crashes with recorded crash pulses.  In Proc. 19^th Int. Techn. Conf. on ESV, Paper No. 05-0363, 1-7
5. Del Grande F., Maus T. P., & Carrino J. A. (2012). Imaging the intervertebral disc: Age-related changes, herniations and radicular pain. Radiological Clinic of North America 50(4), 629-649
6. Issacson, B. M., & Bloebaum, R. D. (2010). Bone electricity: What have we learned in the past 160 years? Journal of Biomedical Research, 95A(4), 1270-1279.
7. Frost, H. M. (1994). Wolff's Law and bone's structural adaptations to mechanical usage: an overview for clinicians. The Angle Orthodontist, 64(3), 175-188.
8. He, G., & Xinghua, Z. (2006). The numerical simulation of osteophyte formation on the edge of the vertebral body using quantitative bone remodeling theory. Joint Bone Spine 73(1), 95-101.

Dr. Mark Studin is an Adjunct Associate Professor of Chiropractic at the University of Bridgeport College of Chiropractic, an Adjunct Professor of Clinical Sciences at Texas Chiropractic College and a clinical presenter for the State of New York at Buffalo, School of Medicine and Biomedical Sciences for post-doctoral education, teaching MRI spine interpretation and triaging trauma cases. Dr. Studin also teaches and coordinates clinical rotations for senior chiropractic interns at the State University of New York at Stony Brook, School, Department of Neuroradiology. He can be reached at DrMark@AcademyofChiropractic.com or www.teachdoctors.com or at 631-786-4253

Dr. Robert Peyster is currently the Chief of Neuroradiology, Associate Chairman of External Radiology and a Professor of Radiology and Neurology at the State University of Stony Brook, School of Medicine after serving as Chief of Neuroradiology at Hahnemann University Hospital in Philadelphia. Dr. Peyster did his radiology and neuroradiology Fellowship training at Harvard’s Massachusetts General Hospital and has been published extensively over the last 40 years while being part of multiple cerebrovascular and brain degenerative clinical trial research. Dr. Peyster also currently trains doctors in multiple disciplines nationally in neuroradiology. Medical-legally, Dr. Peyster has testified 100’s of times for both plaintiff and defense nationally. He can be reached at Bob@Peyster.com or 631-379-0714

Dr. Bill Owens is presently in private practice in Buffalo and Rochester NY and works directly with the emergency departments of SUNY Buffalo Hospitals. He is an Associate Adjunct Professor at the State University of New York at Buffalo School of Medicine and Biomedical Sciences teaching and coordinating clinical rotations for primary care medical providers and medical neurology residents 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 dr.owens@academyofchiropractic.com or www.mdreferralprogram.com or 716-228-3847

Patrick Sundby has decades of experience in the automotive industry including several years in law enforcement collision investigation. He has also been a driver training and firearms instructor in law enforcement and a police officer for 9 years before specializing in accident investigations. He has been trained and was an instructor at Prince William County Criminal Justice Training Academy in Virginia and studied at the Federal Law Enforcement Training Center in Georgia. His specialty is low speed and catastrophic crashes and has testified over 500 times at various levels. He can be reached at 571-265-8076 or patrick.sundby@gmail.com