Low-Speed Damages and Injuries


Patrick Sundby, Accident Investigator



We have discussed the fallacy of “no damage = no injury” in depth in other papers, but as a reminder, we are interested in the relationship between injury and force experience, not damage induced. The phrase “no damage, no injury” is no more than “deceptive rhetoric” and draws a false causal relationship because it is based in subjective interpretation, dogmatic beliefs and too often, who is paying for your opinion. The extent of the damage, as viewed by each person, varies based on each person’s perspective. For example, what color is the square on the left?


What color is the square on the right?

The majority of the viewers of this article should say the squares are blue, but is it possible someone else sees the colors differently? What if this article was read in print form in black and white? What if the screen settings on a reader’s computer were out of adjustment? What if a reader has a condition which alters the way they see certain colors?

Taking the last variable, if the person with the condition sees the squares as something other than blue, are they wrong? No. To him/her, they genuinely see something else. This example demonstrates the subjective interpretation of the two colors presented to you in the squares.

So how do you resolve this subjective approach to the colors? You need to use an objective standard to gauge the colors against thus allowing you to determine if the colors presented are indeed blue.

In the electromagnetic spectrum, there is a small window in which visible light is located.

Within this small window, modern science has defined the wavelengths of different colors.

Rather than debating the colors of the two squares we can measure the wavelengths and compare them to the objective standard if both squares measure between 450 and 495 nm (nanometers) then both squares are indeed blue.

In the same sense of objectively defining colors, we need to objectively define the relationship between damage and injury. This relationship is defined, objectively, through force. If we can quantify the forces exerted on the vehicle (and by extension the occupant), then we can objectively compare those forces to known standards for injury. This MUST BE the method for defining the causal relationship between a vehicle collision and occupant injury vs. relying on dogma, rhetoric and financially influenced opinions because it relies on physics and the inherent mathematical facts.

Imagine being in a high-risk category for cancer and when at an appointment the doctor stands back, looks you up and down - while clothed, and says “you don’t look sick therefore you don’t have cancer.” This is the same practice when reconstruction is done via an insurance estimate. Ask yourself, how can you possibly know the extent of the damage to a vehicle when you didn’t even remove the bumper cover? When we consider the recent Allstate’s “QuickFoto Claim” where you take a picture of the accident, and they send you a check is a brilliant business move. The unsuspecting claimant thinks that getting a check quickly is a resolution of the damages to their car without ever inspecting the damages below the “skin of the car.”

When considering transference of forces and potential bodily injury, after a complete vehicle exam is done, we can assign a known value for the vehicles change in acceleration. This process can take place via a few avenues. For the sake of this paper and topic, we are going to use the Coefficient of Restitution (CoR).


If we can determine the post-impact speeds, we can then mathematically work the pre-impact speed for the striking vehicle thus eliminating any unknowns. Finally, we can check the work and ask if the results appear reasonable. (Remember 30 divided by 100 is also .3)

Consider the following case:

In this event, we have a typical lower speed collision. This vehicle was rear-ended while stopped and the occupant suffered injury. Further, there is the ever-present claim that “little/no damage = no injury.”

There is clear damage to the bumper cover and rear liftgate as well as some panel fitment issues at the corners. I’m highly suspect if we examined the structure of the bumper, we would find more evidence of the collision, and this would further support an appropriate CoR. After an examination of the vehicle, we could reasonably assign a high CoR to this event and work backward to the striking vehicle’s impact speed. While this would be of interest and worth exploring, we have complete tasks similar to this in previous discussions. This collision is important as there is a second and more specific point highlight. Consider the interior shot of this vehicle.

Consider what the chunk of missing steering wheel tells us. First, we know your average person doesn’t have the strength to tear the steering wheel. We can conclude the force of the collision did this, but how? The occupant was holding the wheel when the vehicle was struck. The collision accelerated the vehicle forward, and the occupant did not move at the same time. Once the occupant had “stretched out,” (the slack or bent arms at rest was gone) the force of the collision was translated to the steering wheel through the occupant. The question is, how much force?

The forces experienced by the steering wheel would be whatever percentage of body weight the occupant had in the torso times the “g-forces” calculated. In simpler terms, if the upper body of the occupant weighed in at “X” pounds, the steering wheel experienced this weight times the g-force. Take a quick second and consider if you had the steering wheel in your hands, what could you do to break it in a similar nature? Jump in it? Have a friend hold one side and pull? What does it really take to do damage like this? This concept is a bit of a trick question, any answer you provide is subjective – lets objectively try to determine the forces at play. This is where you put aside pre-conceived “beliefs” and allow the mathematics of physics to render answers because there are no beliefs in math equations.

When we examine the nature of a low-speed event, we will have to determine the g-forces the occupant experiences. For this example, we will utilize the following the following equation:

Initially, it appears very high values can be substituted, and the formula would still be correct. However, this doesn’t pass a sanity test. While the striking vehicle is not provided, we are assuming it’s the same or negligibly different from the KIA. We know the collision is not 100% efficient so the post-impact speed of vehicle two being 10 mph is not reasonable. In the same sense, the post-impact speed for vehicle one being zero is also not reasonable. (WHY?) We are going to use eight and two, respectively.

If the KIA was accelerated to 8 mph (11.76 fps), we could determine the g-forces be 3.65 at the lumbar spine. We also know the forces experienced at the cervical spine can be two to three times more than the lumbar, 7.3 to 10.95, respectively. These forces greatly exceed a plethora of known standards for cervical spine injury.

The process we just went through provides an objective conclusion for the forces that acted on the vehicle, and ALL of these values are a reasonable fit for the damage profile.

There is one final consideration, the broken steering wheel. The occupant holding the steering wheel would have forces act on them differently likely resulting in different injuries or increasing the forces acting on the body. A case-by-case evaluation for each collision and each occupant is a necessity to thoroughly and accurately establish the objective relationship between the forces the vehicle experienced and the forces the occupant experienced – Indeed, “no damage = no injury” is a myth.

Share this

Submit to DeliciousSubmit to DiggSubmit to FacebookSubmit to Google BookmarksSubmit to StumbleuponSubmit to TechnoratiSubmit to TwitterSubmit to LinkedIn

Traumatic Ligament Laxity of the Spine and

Associated Physical Impairment

Lawrence Lefcort, DC


Author Note

            Correspondence concerning this article should be addressed to Lawrence Lefcort, DC at

Bayside Physical Therapy, Chiropractic, and Acupuncture, PLLC, 213-15 33rd Road Bayside,

NY 11361




This paper explores the relationship between traumatic ligament laxity of the spine and the

resultant instability that may occur. Within, there is a discussion of the various spinal

ligamentous structures that may be affected by both macro and micro traumatic events, as

well as the neurologic and musculoskeletal effects of instability. There is detailed discussion of

the diagnosis, quantification, and documentation as well.

            Keywords: ligament laxity, instability




Traumatic Ligament Laxity of the Spine and

Associated Physical Impairment

            Soft tissue cervical and lumbar sprain/strains are the most common injury in motor vehicle collisions, with 28% to 53% of collision victims sustaining this type of injury (Galasko et al., 1993; Quinlan et al., 2000). The annual societal costs of these injuries in the United States are estimated to be between 4.5 and 8 billion dollars (Kleinberger et al., 2000; Zuby et al., 2010). Soft tissue injuries of the spinal column very often become chronic, with the development of long-term symptoms, which can inevitably adversely affect the victim’s quality of life. Research has indicated that 24% of motor vehicle collision victims have symptoms 1 year after an accident and 18% after 2 years (Quinlan et al., 2004). Additionally, it has been found that between 38% and 52% of motor vehicle collision cases involved rear-impact scenarios

( Kleinberger et al.,2000; Galasko et al., 1993).

            It is well known that the major cause of chronic pain due to these injuries is directly related to the laxity of spinal ligamentous structures (Ivancic, et al., 2008). One must fully understand the structure and function of ligaments in order to realize the effects of traumatic ligament laxity. Ligaments are fibrous bands or sheets of connective tissue which link two or more bones, cartilages, or structures together. We know that one or more ligaments provide stability to a joint during rest as well as movement. Excessive movements such as hyper-extension or hyper-flexion, which occur during a traumatic event such as a motor vehicle collision, may be restricted by ligaments, unless these forces are beyond the tensile-strength of these structures; this will be discussed later in this paper.


            Three of the more important ligaments in the spine are the ligamentum flavum, the anterior longitudinal ligament, and the posterior longitudinal ligament (Gray’s Anatomy, 40th Edition). The ligamentum flavum forms a cover over the dura mater, which is a layer of tissue that protects the spinal cord. This ligament connects under the facet joints to create a small curtain, so to speak, over the posterior openings between vertebrae (Gray’s Anatomy, 40th edition). The anterior longitudinal ligament attaches to the front (anterior) of each vertebra and runs vertical or longitudinal (Gray’s Anatomy, 40th edition). The posterior longitudinal ligament also runs vertically or longitudinally behind (posterior) the spine and inside the spinal canal (Gray’s Anatomy, 40th Edition). Additional ligaments include facet capsular ligaments, interspinous ligaments, supraspinous ligaments, and intertransverse ligaments. The aforementioned ligaments limit flexion and extension, with the exception of the ligament, which limits lateral flexion. The ligamentum nuchae, which is a fibrous membrane, limits flexion of the cervical spine (Gray’s Anatomy, 40th Edition). The four ligaments of the sacroiliac joints

(iliolumbar, sacroiliac, sacrospinus, sacrotuberous), provide stability and some motion. The upper cervical spine has its own ligamentous structures or systems; occipitoatlantal ligament complex, occipitoaxial ligament complex, atlantoaxial ligament complex, and the cruciate ligament complex (Gray’s Anatomy, 40th Edition). The upper cervical ligament system is especially important in stabilizing the upper cervical spine from the skull to C2 (axis) (Stanley Hoppenfeld, 1976). It is important to note, that although the cervical vertebrae are the smallest, the neck has the greatest range of motion.


            Ligament laxity may happen as a result of a ‘macro trauma”, such as a motor vehicle collision, or may develop overtime as a result of repetitive use injuries, or work-related injuries. The cause of this laxity develops through similar mechanisms, which leads to excessive motion of the facet joints, and will cause various degrees of physical impairment. When ligament laxity develops over time, it is defined as “creep” and refers to the elongation of a ligament under a constant or repetitive stress (Frank CB, 2004). Low-level ligament injuries, or those where the ligaments are simply elongated, represent the vast majority of cases and can potentially incapacitate a patient due to disabling pain, vertigo, tinnitus, etc.. Unfortunately, these types of strains may progress to sub-failure tears of ligament fibers, which will lead to instability at the level of facet joints (Chen HB et al., 2009). Traumatic or repetitive causes of ligament laxity will ultimately produce abnormal motion and function between vertebrae under normal physiological loads, inducing irritation to nerves, possible structural deformation, and/or incapacitating pain.

            Patients’, who have suffered a motor vehicle collision or perhaps a work-related injury, very often have chronic pain syndromes due to ligament laxity. The ligaments surrounding the facet joints of the spinal column, known as capsular ligaments, are highly innervated mechanoreceptive and nociceptive free nerve endings. Therefore, the facet joint is thought of as the primary source of chronic spinal pain (Boswell MV et al., 2007; Barnsley L et al., 1995). When the mechanoreceptors and nociceptors are injured or even simply irritated the overall joint function of the facet joints are altered (McLain RF, 1993).


            One must realize that instability is not similar to hyper-mobility. Instability, in the clinical context, implies a pathological condition with associated symptomatology, whereas joint hypermobility alone, does not. Ligament laxity which produces instability refers to a loss of “motion stiffness”, so to speak, in a particular spinal segment when a force is applied to this segment, which produces a greater displacement than would be observed in a normal motion segment. When instability is present, pain and muscular spasm can be experienced within the patient’s range of motion and not just at the joint’s end-point. In Chiropractic, we understand that there is a “guarding mechanism”, which is triggered after an injury, which is the muscle spasm. These muscle spasms can cause intense pain and are the body’s response to instability, since the spinal supporting structures, the ligamentous structures, act as sensory organs, which initiate a ligament-muscular reflex. This reflex is a “protective reflex” or “guarding mechanism”, produced by the mechanoreceptors of the joint capsule and these nerve impulses are ultimately transmitted to the muscles. Activation of surrounding musculature, or guarding, will help to maintain or preserve joint stability, either directly by muscles crossing the joint or indirectly by muscles that do not cross the joint, but limit joint motion (Hauser RA et al., 2013). This reflex is fundamental to the understanding of traumatic injuries.

            This reflex is designed to prevent further injury. However, the continued feedback and reinforcement of pain and muscle spasm, will delay the healing process. The ‘perpetual loop” may continue for a long period of time, making further injury more likely due to muscle contraction. Disrupting this cycle of pain and inflammation is key to resolution.


            When traumatic ligament laxity produces joint instability, with neurologic compromise, it is understood that the joint has sustained considerable damage to its stabilizing structures, which could include the vertebrae themselves. However, research indicates that joints that are hypermobile demonstrate increased segmental mobility, but are still able to maintain their stability and function normally under physiological loads (Bergmann TF et al., 1993).

            Clinicians classify instability into 3 categories, mild, moderate, and severe. Severe instability is associated with a catastrophic injury, such as a motor vehicle collision. Mild or moderate clinical instability is usually without neurologic injury and is most commonly due to cumulative micro-trauma, such as those associated with repetitive use injuries; prolonged sitting, standing, flexed postures, etc..

            In a motor vehicle collision, up to 10 times more force is absorbed in the capsular ligaments versus the intervertebral disc (Ivancic PC et al., 2007). This is true, because unlike the disc, the facet joint has a much smaller area in which to disperse this force. Ultimately, as previously discussed, the capsular ligaments become elongated, resulting in abnormal motion in the affected spinal segments (Ivancic PC et al., 2007; Tominaga Y et al., 2006). This sequence has been clearly documented with both in vitro and in vivo studies of segmental motion characteristics after torsional loads and resultant disc degeneration (Stokes IA et al., 1987; Veres SP et al., 2010). Injury to the facet joints and capsular ligaments has been further confirmed during simulated whiplash traumas (Winkelstein BA et al., 2000).


            Maximum ligament strains occur during shear forces, such as when a force is applied while the head is rotated (axial rotation). While capsular ligament injury in the upper cervical spine region can occur from compressive forces alone, exertion from a combination of shear, compression and bending forces is more likely and usually involves much lower loads to causes injury (Siegmund GP et al., 2001). If the head is turned during whiplash trauma, the peak strain on the cervical facet joints and capsular ligaments can increase by 34% (Siegmund GP et al., 2008). One research study reported that during an automobile rear-impact simulation, the magnitude of the joint capsule strain was 47% to 196% higher in instances when the head was rotated 60 degrees during impact compared with those when the head was forward facing (Storvik SG et al., 2011). Head rotation to 60 degrees is similar to an individual turning his/her head to one side while checking for on-coming traffic and suddenly experiences a rear-end collision. The impact was greatest in the ipsilateral facet joints, such that head rotation to the left caused higher ligament strain at the left facet joint capsule.

            Other research has illustrated that motor vehicle collision trauma has been shown to reduce ligament strength (i.e., failure force and average energy absorption capacity) compared with controls or computational models (Ivancic PC et al., 2007; Tominaga Y et al., 2006). We know that this is particularly true in the case of capsular ligaments, since this type of trauma causes capsular ligament laxity. Interestingly, one research study conclusively demonstrated that whiplash injury to the capsular ligaments resulted in an 85% to 275% increase in ligament elongation (laxity), compared to that of controls (Ivancic PC et al., 2007).


The study also reported evidence that tension of the capsular ligaments due to trauma, requisite for producing pain from the facet joint. Whiplash injuries cause compression injuries to the posterior facet cartilage. This injury also results in trauma to the synovial folds, bleeding, inflammation, and of course pain. Simply stated, this stretching injury to the facet capsular ligaments will result in joint laxity and instability.

            Traumatic ligament laxity resulting in instability is a diagnosis based primarily on a patient’s history (symptoms) and physical examination. Subjective findings are the patient’s complaints in their own words, or their perception of pain, sensory changes, motor changes, or range of motion alterations. After the patient presents their subjective complaints to the clinician, these subjective findings, must be correlated and confirmed through a proper and thorough physical examination, including the utilization of imaging diagnostics that explain a particular symptom, pattern, or area of complaint objectively. Without some sort of concrete evidence that explains a patient’s condition, we merely have symptoms with no forensic evidence. Documentation is key, as well as quantifying the patient’s injuries objectively.

            In order to adequately quantify the presence of instability due to ligament laxity, the clinician could utilize functional computerized tomography, functional magnetic resonance imaging scans, as well as digital motion x-ray (Radcliff K et al., 2012; Hino H et al., 1999). Studies using functional CT for diagnosing ligamentous injuries have demonstrated the ability of this technique to shoe excess movement during axial rotation of the cervical spine (Dvorak J et al., 1988; Antinnes J et al., 1994).             


This is important to realize when patients have the signs and symptoms of instability, but have normal MRI findings in the neutral position. Functional imaging technology, as opposed to static standard films, is necessary for the adequate radiologic depiction of instability because they provide dynamic imaging during movement and are extremely helpful for evaluating the presence and degree of instability.

            Although functional imaging maybe superior plain-film radiography is still a powerful diagnostic tool for the evaluation of instability due to ligament laxity. When a patient presents status-post motor vehicle collision, it is common practice to perform a “Davis Series” of the cervical spine. This x-ray series consists of 7 views: anterior-posterior open mouth, anterior-posterior, lateral, oblique views, and flexion-extension views. The lumbar spine is treated in similar fashion. X-ray views will include: anterior-posterior, lateral, oblique views, and flexion-extension views. The flexion-extension views are key in the diagnosis of instability. It is well known, that the dominant motion of the cervical and lumbar spine, where most pathological changes occur, is flexion-extension. Translation of one vertebral segment in relation to the one above and/or below will be most evident on these views. Translation is the total anterior-posterior movement of vertebral segments. After the appropriate views are taken, the images may be evaluated utilizing CRMA or Computed Radiographic Mensuration Analysis. These measurements are taken to determine the presence of ligament laxity. In the cervical spine, a 3.5mm or greater translation of one vertebra on another is an abnormal and ratable finding, indicative of instability (AMA Guides to the Evaluation of Permanent Impairment, 6th Edition).


            Alteration of Motion Segment Integrity (AOMSI) is extremely crucial as it relates to ligament laxity. The AMA Guides to the Evaluation of Permanent Impairment 6th Edition, recognize linear stress views of radiographs, as the best form of diagnosing George’s Line

(Yochum & Rowe’s Essentials of Radiology, page 149), which states that if there is a break in George’s Line on a radiograph, this could be a radiographic sign of instability due to ligament laxity.

            Our discussion of ligament laxity and instability continues with the “Criteria for Rating Impairment Due to Cervical and Lumbar Disorders”, as described in the AMA Guides to the Evaluation of Permanent Impairment, 6th Edition. According to the guidelines, a DRE (Diagnosed Related Estimate) Cervical Category IV is considered to be a 25% to 28% impairment of the whole person. Category IV is described as, “alteration of motion segment integrity or bilateral or multilevel radiculopathy; alteration of motion segment integrity is defined from flexion and extension radiographs, as at least 3.5mm of translation of one vertebra on another, or angular motion of more than 11 degrees greater than at each adjacent level; alternatively, the individual may have loss of motion of a motion segment due to a developmental fusion or successful or unsuccessful attempt at surgical arthrodesis; radiculopathy as defined in Cervical Category III need not be present if there is alteration of motion segment integrity; or fractures: (1) more than 50% compression of one vertebral body without residual neural compromise. One can compare a 25% to 28% cervical impairment of the whole person to the 22% to 23% whole person impairment due to an amputation at the level of the thumb at or near the carpometacarpal joint or the distal third of the first metacarpal.


            Additionally, according to the guidelines, a DRE (Diagnosed Related Estimate) Lumbar Category IV is considered to be a 20% to 23% impairment of the whole person. Category IV is described as, “loss of motion segment integrity defined from flexion and extension radiographs as at least 4.5mm of translation of one vertebra on another or angular motion greater than 15 degrees at L1-2, L2-3, and L3-4, greater than 20 degrees at L4-5, and greater than 25 degrees at L5-S1; may have complete or near complete loss of motion of a motion segment due to developmental fusion, or successful or unsuccessful attempt at surgical arthrodesis or fractures: (1) greater than 50% compression of one vertebral body without residual neurologic compromise. One can compare a 20% to 23% Lumbar Impairment of the whole person to the 20% whole person impairment due to an amputation of the first metatarsal bone.  


            After careful interpretation of the AMA Guides to the Evaluation of Permanent Impairment, 6th Edition, regarding whole person impairment due to ligament laxity/instability of the cervical and lumbar spine, one can certainly see the severity and degree of disability that occurs. Once ligament laxity is correctly diagnosed, it will objectively quantify a patient’s spinal injury regardless of symptoms, disc lesions, range of motion, reflexes, etc. When we quantify the presence of ligament laxity, we also provide a crucial element with which to demonstrate instabilities in a specific region. Overall, clarification and quantification of traumatic ligament laxity will help the patient legally, objectively, and most importantly, clinically.  


AMA Guides to the Evaluation of Permanent Impairment, 6th Edition

Antinnes J, Dvorak J, Hayek J, Panjabi MM, Grob D. The value of functional computed tomography in the evaluation of soft-tissue injury in the upper cervical spine. Eur Spine J. 1994; 98-101. [PubMed]

Barnsley L, Lord SM, Wallis BJ, Bogduk N. The prevalence of cervical zygapophaseal joint pain after whiplash. Spine (Phila Pa 1976). 1995;20: 20-5. [PubMed]

Bergmann TF, Peterson DH. Chiropractic technique principles and procedures, 3rd ed. New York Mobby Inc. 1993

Boswell MV, Colson JD, Sehgal N, Dunbar EE, Epter R. A systematic review of therapeutic facet joint interventions in chronic spinal pain. Pain Physician. 2007;10(1): 229-53. [PubMed]

Chen HB, Yang KH, Wang ZG. Biomechanics of whiplash injury. Chin J Traumatol.2009;12(5): 305-14. [PubMed]

Dvorak J, Penning L, Hayek J, Panjabi MM, Grob D, Zehnder R. Functional diagnostics of the cervical spine using computer tomography. Neuroradiology. 1988;30: 132-7. [PubMed]

Examination of the Spine and Extremities, Stanley Hoppenfeld, 1976

Frank CB. Ligament structure, physiology, and function. J Musculoskelet Neuronal Interact. 2004;4(2): 199-201. [PubMed]

Galasko, C.S., P.M. Murray, M. Pitcher, H. Chanter, S. Mansfield, M. Madden, et. al Neck sprains after road traffic accidents: a modern epidemic. Injury 24(3): 155-157, 1993

American Medical Association. (2009). Guides to the evaluation of permanent impairment,

            6th edition. Chicago, Il:AMA

Antinnes, J., Dvorak, J., Hayek, J., Panjabi, M.M., & grob, D. (1994). The value of functional

            Computed tomography in the evaluation of soft tissue injury in the upper cervical

            spine. European Spine Journal, 98-101.

Barnsley, L., Lord, S.M., Wallis, B.J., & Bogduk, N. (1995). The prevalence of cervical zygaphaseal

            joint pain after whiplash. Spine, 20, 20-25.

Bergmann, T.F., & Peterson, D.H. (1993). Chiropractic technique principles and procedures,

            3rd edition. New York: Mobby Inc.

Boswell, M.V., Colson, J.D., Sehgal, N., Dunbar, E.E., & Epter, R. (2007). A symptomatic review

            of therapeutic facet joint interventions in chronic spinal pain. Pain Physician, 10(1),


Chen, H.B., Yang, K.H., & Wang, Z.G. (2009). Biomechanics of whiplash injury. Chinese Journal

            Traumatol, 12(5), 305-314.

Dvorak, J., Penning, L., Hayek, J., Panjabi, M.M., Grob, D., & Zehnder, R. (1988). Functional

diagnostics of the cervical spine using computer tomography. Neuroradiology, 30, 132-


Frank, C.B. (2004). Ligament structure, physiology, and function. Musculoskeletal Neuronal

            Interaction, 4, 199-201.

Galasko, C.S., Murray, P.M., Pitcher, M., Chantar, S., & Mansfield, M. (1993). Neck sprains after

            road traffic accidents: A modern epidemic. Injury, 24(3), 155-157.

Gray, H. (2008). Gray’s anatomy. London: Churchill Livingstone/Elsevier.

Hoppenfeld, S. (1976). Physical examination of the spine and extremities. East Norwalk, CT:


Ivancic, P.C., Coe, M.P., & Ndu, A.B. (2007). Dynamic mechanical properties of intact human

            cervical ligaments. Spine Journal, 7(6), 659-665.

Ivancic, P.C., Ito, S., Tominaga, Y., Rubin, W., Coe, M.P., Ndu, A.B., et al. (2008). Whiplash causes

            Increased laxity of cervical capsular ligament. Clinical Biomechanics (Bristol Avon).

Kleinberger, M. (2000). Frontiers in whiplash trauma. Amsterdam: ISO Press.

Siegmund, G.P., Davis, M.B., & Quinn, K.P. (2008). Head-turned postures increase the risk of

            cervical facet capsule injury during whiplash. Spine, 33(15), 1643-1649.

Siegmund, G.P., Meyers, B.S., Davis, M.B., Bohnet, H.F., & Winkelstein, B.A. (2001). Mechanical

            evidence of cervical facet capsule injury during whiplash, a cadaveric study using

            combined shear, compression, and extension loading. Spine, 26(19), 2095-2101.

Stokes, I.A., & Frymoyer, J.W. (1987). Segmental motion and instability. Spine, 7, 688-691.

Storvik, S.G., & Stemper, B.D. (2011). Axial head rotation increases facet joint capsular ligament

            strains in automotive rear impact. Medical Bioengineeering Comput., 49(2), 153-161.

Tominaga, Y., Ndu, A.B., & Coe, M.P. (2006). Neck ligament strength is decreased following

            whiplash trauma. BMC Musculoskeletal Disorders, 7, 103.

Veres, S.P., Robertson, P.A., & Broom, N.D. (2010). The influence of torsion on disc herniation

            when combined with flexion. European Spine Journal, 19, 1468-1478.

Winkelstein, B.A., Nightingale, R.W., Richardson, W.J., & Myers, B.S. (2000). The cervical

facet capsule and its role in whiplash injury: A biomechanical investigation. Spine,

25(10), 1238-1246.  





Share this

Submit to DeliciousSubmit to DiggSubmit to FacebookSubmit to Google BookmarksSubmit to StumbleuponSubmit to TechnoratiSubmit to TwitterSubmit to LinkedIn

Strain/Sprain is ONE Syndrome

Not Two Separate Pathologies

And Is Permanent



William J. Owens DC, DAAMLP


Citation: Studin M., Owens W. (2017) Strain/Sprain Is One Syndrome, Not 2 Separate Pathologies and is Permanent, American Chiropractor 39 (2) 26, 28, 30-31


According to the National Institute of Health’s, National Institute of Arthritis and Musculoskeletal and Skin Disorders:

A sprain is an injury to a ligament (tissue that connects two or more bones at a joint). In a sprain, one or more ligaments is stretched or torn. A strain is an injury to a muscle or a tendon (tissue that connects muscle to bone). In a strain, a muscle or tendon is stretched or torn. (https://www.niams.nih.gov/health_info/sprains_strains/sprains_and_strains_ff.asp)


Historically, doctors of all disciplines in the clinical setting and lawyers in the medical-legal arena have erroneously attempted to separate them into 2 distinct injuries allowing a false conclusion to be derived in either prognosis or legal arguments when considering connective tissue pathology as sequella to trauma.



Solomonow (2009) wrote:

There are several ligaments in every joint in the human skeleton and they are considered as the primary restraints of the bones constituting the joint. Ligaments are also sensory organs and have significant input to sensation and reflexive/synergistic activation of muscles. The muscles associated with any given joint, therefore, also have a significant role as restraints. In some joints, such as the intervertebral joints of the spine, the role of the muscles as restraints is amplified. The role of ligaments as joint restraints is rather complex when considering the multitude of physical activities performed by individuals in routine daily functions, work and sports, the complexity of the anatomy of the different joints and the wide range of magnitude and velocity of the external loads. As joints go through their range of motion, with or without external load, the ligaments ensure that the bones associated with the joint travel in their prescribed anatomical tracks, keep full and even contact pressure of the articular surfaces, prevent separation of the bones from each other by increasing their tension, as may be necessary, and ensuring stable motion. Joint stability, therefore, is the general role of ligaments without which the joint may subluxate, cause damage to the capsule, cartilage, tendons, nearby nerves and blood vessels, discs (if considering spinal joints) and to the ligaments themselves. Such injury may debilitate the individual by preventing or limiting his/her use of the joint and the loss of function. Pgs. 136-137


While ligaments are primarily known as mechanical or supportive structures responsible for joint stability, they have equally important neurological functions. Anatomical studies have shown that ligaments in the extremities and the spine are endowed with nerves called mechanoreceptors. The presence of such that sense and send neurological information to the spine and brain in the ligaments confirms that they contribute to proprioception (feeling and analyzes one’s physical positon in space and time) and kinesthesia (similar to proprioception but can maintain feeling in these nerves even with aberrant neurological imput elsewhere) and also has a distinct role in reflex activation or inhibition of muscular activities.


Simply put, the nerves in ligaments attempts to alter muscle activity to prevent further biomechanical failure and pathology (bodily injury), which effects one’s ability to move in a balanced homeostatic manner leading to further functional loss in a short amount of time. The presence of such nerves in the ligaments confirms that they contribute to proprioception and kinesthesia and have a distinct role in reflex activation or inhibition of muscular activities. Therefore, the muscles and tendons (which are inherent in muscular activity), are responsive and dependent upon ligament activity in function with both normal and pathological (inclusive of trauma) activities.  


Solomonow (2009) also reported that as far back as the turn of the last century, that a reflex may exist from sensory receptors in the ligaments to muscles that may directly or indirectly modify the load imposed on the ligament. A clear demonstration of a reflex activation of muscles finally provided in 1987 and reconfirmed several times since then. It was further shown that such a ligamento-muscular reflex exists in most extremity joints and in the spine.


A Single trauma according to Panjabi (2006) can cause either a tear in the ligament called laxity or a subfailure injury of the spinal ligaments and injury to the mechanoreceptors embedded in the ligaments and the following cascade of events occur: pgs. 669-670


NOTE: The subfailure injury of the spinal ligament is defined as an injury caused by stretching of the tissue beyond its physiological limit, but less than its failure point.


  1. When the injured spine performs a task or it is challenged by an external load, the transducer signals generated by the mechanoreceptors are corrupted.
  2. Neuromuscular control unit has difficulty in interpreting the corrupted transducer signals because there is spatial and temporal mismatch between the normally expected and the corrupted signals received.
  3. The muscle response pattern generated by the neuromuscular control unit is corrupted, affecting the spatial and temporal coordination and activation of each spinal muscle.
  4. The corrupted muscle response pattern leads to corrupted feedback to the control unit via tendon organs of muscles and injured mechanoreceptors, further corrupting the muscle response pattern.
  5. The corrupted muscle response pattern produces high stresses and strains in spinal components leading to further subfailure injury of the spinal ligaments, mechanoreceptors and muscles, and overload of facet joints.
  6. The abnormal stresses and strains produce inflammation of spinal tissues, which have abundant supply of nociceptive sensors and neural structures.
  7. Consequently, over time, chronic biomechanical failure develops leading to premature degeneration and long-term pain.

Simply explained, when there is a ligament injury or sprain, the nerves in the ligament fire signals that go to the central nervous system and causes the muscles to react as compensation to bodily injury to stabilize the structure. That in turn sets up another cascade of problems if not compensated for or repaired as the muscle spasticity cannot maintain itself for long periods of time and goes into a posture of tetanus, or perpetual spasm until the lactic acid builds. This is followed by the muscle failing and putting the entire structure in a chronic biomechanically unstable position and causing the bone to remodel or become arthritic. 


According to Hauser ET. Al (2013) ligament instability in either subfailures or laxity are a clear cause of osteoarthritis. This is not speculative as the inured will develop arthritis in 100% of the time and is consistent with Wolff’s Law that has been, and continues to be accepted since the late 18th century. 


Therefore, as per the above scenario, strain-sprain is an intertwined syndrome that cannot either mechanically or neurologically be separated and will cause arthritis in 100% of the post-trauma instance. How much arthritis and how quickly it will develop is dependent upon how much ligamentous damage there is.  



  1. What Are Sprains and Strains? National Institute of Health, National Institute of Arthritis and Musculoskeletal and Skin Disorders (2016) Retrieved from:(https://www.niams.nih.gov/health_info/sprains_strains/sprains_and_strains_ff.asp)
  2. Solomonow, M. (2009). Ligaments: a source of musculoskeletal disorders.Journal of Bodywork and Movement Therapies,13(2), 136-154.
  3. Panjabi, M. M. (2006). A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction.European Spine Journal,15(5), 668-676.
  4. Hauser R., Dolan E., Phillips H., Newlin A., Moore R., Woldin B., Ligament & Healing Injuries: A Review of Current Clinical Diagnostics and Therapeutics, The Open Rehabilitation Journal, 2013, 6, 1-20



Dr. Mark Studin (CLICK HERE FOR CV) 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, spinal biomechanical engineering and triaging trauma cases. He also coordinates a clinical rotation in neuroradiology for chiropractic students at the State University of New York at Stony Brook, School of Medicine, Department of Radiology. Dr. Studin is also the president of the Academy of Chiropractic teaching doctors of chiropractic how to interface with the medical and legal communities (www.DoctorsPIProgram.com), teaches MRI interpretation and triaging trauma cases to doctors of all disciplines nationally and studies trends in healthcare on a national scale (www.TeachDoctors.com). 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 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 dr.owens@academyofchiropractic.com or www.mdreferralprogram.com or 716-228-3847  

Share this

Submit to DeliciousSubmit to DiggSubmit to FacebookSubmit to Google BookmarksSubmit to StumbleuponSubmit to TechnoratiSubmit to TwitterSubmit to LinkedIn

Ligament Failure and Strain-Sprain Reported as Permanent in Whiplash



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.




  1. Cocchiarella L., Anderson G., (2001) Guides to the Evaluation of Permanent Impairment, 5th Edition, Chicago IL, AMA Press
  2. Juamard N., Welch W., Winkelstein B. (July 2011) Spinal Facet Joint Biomechanics and Mechanotransduction in Normal, Injury and Degenerative Conditions, Journal of Biomechanical Engineering, 133, 1-31


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 dr.owens@academyofchiropractic.com or www.mdreferralprogram.com or 716-228-3847

Share this

Submit to DeliciousSubmit to DiggSubmit to FacebookSubmit to Google BookmarksSubmit to StumbleuponSubmit to TechnoratiSubmit to TwitterSubmit to LinkedIn

Ligament Pathology as Sequella to Trauma Coupled with Alteration of Motion Segment Integrity (AOMSI) or Ligamentous Laxity


By: Ray Wiegand, D.C.



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.




  1. White, et al., Clin Ortho Relat Res, 1975;(109):85-96
  2. Hauser, Dolan,Phillips, Newlin, Moore Woldin, B.A.(2013) Ligament injury and healing: A review of current clinical diagnostics and therapeutics.The Open Rehabilitation Journal, 6,1-20.

Share this

Submit to DeliciousSubmit to DiggSubmit to FacebookSubmit to Google BookmarksSubmit to StumbleuponSubmit to TechnoratiSubmit to TwitterSubmit to LinkedIn