Ligament Failure and Strain-Sprain Reported as Permanent in Whiplash
By: Mark Studin DC, FASBE(C), DAAPM, DAAMLP
William J. Owens DC, DAAMLP
When we investigate the aberrant sequela to victims in car crashes, providers often overlook and concurrently underestimate the tissue pathology and resultant biomechanical failures of spinal ligamentous damages commonly known as “strain – sprain.” In addition, the courts have been “blinded” by rhetoric in allowing this pathology to be deemed transient. There is an ever growing body of scientific literature that verifies strain - sprain as permanent pathology, which is the standard being taught in today’s medical and chiropractic academia. In addition, strain – sprain as sequela to whiplash in the majority of cases, renders a 25% whole person impairment based upon the American Medical Association’s Guide to the Evaluation of Permanent Impairment fifth and sixth editions.
Juamard, Welch and Winkelstein (2011) reported:
“…Rear end accelerations have been used to study the response of a variety of soft tissues in the cervical spine, including the facet capsular ligament. For simulations of whiplash exposures, the strains in the capsular ligament were found to be two – five times greater than those sustained during physiological motions of the cervical spine. In a similar but separate study, the facet joints of the cervical spine’s that were previously exposed to a whiplash injury ridden exercise under low – level tension and found to undergo elongations nearly 3 times greater than on exposed ligaments for the same tensile loads. Those capsular ligaments were also found to exhibit greater laxity after the purported injury. Since increased laxity may be linked to a reduction in the joints ability to stabilize the motion segment during sagittal motion, this finding suggests that whiplash exposure may alter the structure of the individual’s tissues of the facet, such as the capsular ligament, and/or the mechanotransduction processes that could maintain and repair the ligamentous structure. Accordingly, such an injury exposure could initiate a variety of signaling cascades that prevent a full recovery of the mechanical properties of the tissues of the facet joint.” (Pg 15)
Simply put, if we focus on the last sentence above, this “prevents a full recovery of the mechanical properties of the tissues of the facet joint,” which is referencing the ligaments of the spine that make up the tissues of the facet joint. In lay terms; it means that once injured, a joint is permanently damaged and it is demonstrable on x-rays with an extension and flexion view that does not have to show a full dislocation. Therein lies the core of the issue. Most radiologists are not trained in the latest literature on biomechanical tissue failures and therefore underreport the pathology.
Last month I attended a presentation by Michael Modic MD, Neuroradiology, a nationally renowned educator in neuroradiology who focuses on spondylolisthesis (vertebral segmental abnormal movements) and I asked a simple question “why don’t radiologist report more on abnormal positioning due to biomechanical failure as a result of ligament pathology” and his answer was “because their training focuses more on disease pathology.” Although I agree that is critical, so are biomechanical failures that lead to chronic degeneration, which is epidemic in our society. Simply look at the posture of our elderly for verification and much of that started with a simple “fender bender” years ago where the strain-sprain was either undiagnosed or deemed transient and not treated.
The above scenario is why the American Medical Association values ligament pathology at 25% whole body impairment. There is also a growing body of doctors who are trained and credentialed in Spinal Biomechanical Engineering that understand how to create a diagnosis and prognosis, along with treatment plans around ligament pathology and fully understand the long-term effects of damaged facet joint tissues. These doctors are currently educating, based upon the current scientific literature their respective radiology communities to be able to diagnose and document the full extent of the injuries sustained.
We must also recognize that there is a significant amount of evidence in the scientific literature that verifies ligamentous damage as permanent and refutes the rhetorical claim of “transient.” In the end, it must be the facts of human physiology verified by science that sets the standards of healthcare and not deceptive rhetoric at any level.
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 at 631-786-4253
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 email@example.com or www.mdreferralprogram.com or 716-228-3847
Ligament Pathology as Sequella to Trauma Coupled with Alteration of Motion Segment Integrity (AOMSI) or Ligamentous Laxity
By: Ray Wiegand, D.C.
Mark Studin DC, FASBE(C), DAAPM, DAAMLP
A good read to understanding alteration of motion segment integrity (AOMSI) is the article “Biomechanical Analysis of clinical instability in the cervical spine” White, et al., Clin Ortho Relat Res, 1975;(109):85-96.
AOMSI is a biomechanical analysis. It’s all about numbers that have clinical meaning and significance. Threshold values have been determined that quantify without a doubt the patient has serious injury. It is a test of structural integrity of the ligaments interconnecting the motion segments. In this case, structural integrity has to do with the material properties of ligament tissue. Those properties include strength and flexibility. When a material is both strong and flexible, it’s called a semi-rigid material. Strength is related to the composition of the material. Strength might be thought of as load carrying capacity before failure.
Ligament tissue has previously been bench tested to describe its physical characteristics of stress/strain. That is, given so much load (stress) how much elongation will occur (strain). During normal physiologic loads the ligament remains intact and recoils to its original length when the load is removed. If the load becomes too large the materials (ligaments) begin to yield. They go past their elastic limit. When this happens the (strained) ligament fibers will not return to their original shape. The ligament loses its restraining capacity to hold the joint in normal stabilization and hypermobility occurs.
The ligaments, if sufficiently strained or avulsed results in AOMSI. The following paragraphs illustrates that if AOMSI is found there must be gross destruction or yielding of multiple ligaments. We need to build a BIG motion segment with Velcro ligaments. When you tear them off, they make a really nice ripping noise. That drives home the point.
In the White et al work, they found that the motion segment stayed intact i.e., less than 11 degrees’ rotation (angualr mtion) and less than 3.5 mm translation, until they transected over 50% of the ligaments from an anterior or posterior approach. And when they transected from either approach the loss of stability was not linear but suddenly catastrophic. And they meant that suddenly the two vertebra totally separated in rotation or translation.
Suddenly Separated: pulled apart, head off of body, all neural components compromised, paralysis. Keeping that in mind, what are the injuries of someone just under the threshold? Severe to very severe. They stand the possibility of a serious event with much less force.
If AOMSI is detected, think about more than 50% of ligaments transected. That will start to explain the seriousness of the finding. In a patient/child that demonstrates hypermobility everywhere, then you take a statistical average of all segments, and look at the aberrant statistical finding if it exists. There are clues to injury everywhere when you understand what the numbers mean in reference to stability and function.
To diagnose ligament laxity, it is imperative that imaging be performed and a basic flexion-extension x-ray is all that is required. In today’s medical economy, advanced imaging of MRI or CT Scan, although accurate becomes an unnecessary expenditure and an x-ray renders very accurate demonstrative images to conclude a definitive diagnosis. In determining if there is an impairment, it is necessary to follow the AMA Guides to the Evaluation of Permanent Impairment as the 4th, 5th and 6th editions all render an impairment for AOMSI as sequella to ligament laxity, which is damage to the ligament from trauma.
This document is intended to serve as a simple explanation as to the severity of ligament damage and how to demonstrably diagnose the injury. It is also critical to remember that ligament do “wound repair.” In normal physiology, ligaments grow during puberty from cells within the ligaments called fibroblasts. They produce both collagen (white) and elastin (yellow) tissue, which gives the ligaments both tensile and elastic strength. Upon puberty the cells stop producing tissue and remains dormant. Upon injury, the fibroblast reactivates, but can only produce collage leaving the joint wound repaired in an aberrant juxtaposition (place) with poor movement abilities due to the lack of the requisite elastin. In turn, according to Hauser et. Al (2013) this leads to permanent loss of function of the ligament and arthritis of the joint. This is not a speculative statement; it is based upon Wolff’s that dates back to the late 1800’s and has been a guiding principle in healthcare for more than a century.