Low-Speed Accidents and Minimal Force Causing Bodily Injury


Patrick Sundby, Accident Investigator




Citation: Sundby P., Studin M. (2019) Low-Speed Accidents and Minimal Force Causing Bodily Injury, American Chiropractor 41(7) 44, 46, 48-49


When considering bodily injury, too often rhetoric or false perception “rules the day” in spite of sound conclusions based upon the mathematics in physics. This is commonly seen in Independent Medical Examination, Defense Medical Examination and in the courtroom. When assigning causality in the clinical setting, most doctors experienced in the diagnosis and management of trauma cases have concluded their patient's bodily injuries are directly related to the specific trauma, but don’t have the tools to render an accurate rationale. To demonstrably conclude the transference of forces from the bullet car to the target car and then to the occupant, you must first understand and then apply the principles of the “forces” involved. There are several components to discussing the forces applied to the occupant in a collision and here we will discuss the two most important, the quantity of forces delivered and how the force is applied.

The quantity of the force? What do we mean when we say that? There are a lot of different scales one could use, so we need one which is reasonably universal and applicable. For this we use “g-forces.” G-Force is a relationship to gravity which can be easily quantified to any event of motion. The odds are good you (the reader) are sitting in a chair, the chair exerts a force on you to keep you from falling to the floor, this force is 1 g. You will experience this force for the entire time you are seated, which opens the second part of the discussion – time.

The g-forces you experience are one part of the issue, the time it takes to experience the force is the second part. Imagine flying in a military jet fighter and the pilot banks the plane into a turn. You will experience an increase in force on your body which is related to the angle of the bank and the radius of the turn – most importantly, you will experience this increase in force for as long as the plane stays in that flight path. If the force is 4 g’s and the plane maintains that path of travel for 10 seconds you will experience the force evenly over the 10 seconds. In most of this example the time doesn’t change.[1]

What happens when there is a time change? What happens when that same fighter jet lands on an aircraft carrier and the arresting wire take the plane from 200 miles per hour to zero in less than 4 seconds? The forces that are translated to the human body (what you feel) can be quantified in g-forces. The calculation is not quite as simple as multiplying the g forces against the time, rather we need to know the change in speed over the change in time. For the sake of discussion let’s say the slowest approach speed for the jet fighter landing on the carrier is 100 mph (147 fps) and it takes 4 seconds for the plane to come to a complete stop.





The math looks like this:



Although we commonly say g’s (meaning g force), there is no unit with this number, rather it’s a ratio of force acceleration against gravity (which is also acceleration) and the units divide out leaving us with just the 1.14. If we were in the plane in the scenario above, we would experience 1.14 times the force of gravity, 1.14 g’s.

We can apply this concept to starting to move from a complete stop. If were sitting in traffic, stopped, and we were struck from behind we would go from zero to a certain speed – let say 8 mph (11.76 fps). If the time to be accelerated took .1 or 1/10th of a second, we can also calculate the g-forces experienced by the occupant and then determine the injury potential. (See below)

The provided value of 3.65 g’s (in the calculation below) is the relationship experienced at the seat base and is not the same force experienced at the skull. We know the research shows the cervical spine and the skull experience approximately three times the force of the hip – why?

As the vehicle begins to move and so does the occupant’s hip, the skull however, isn’t moving just yet. After all the “slack” in the lumbar and thoracic spine is used the skull and cervical spine are all that’s left, and it takes time to use the slack in the lumbar and thoracic spine resulting in less time for the cervical spine and skull. As a demonstration of concept – if we said it takes 66% of the 1/10th of a second to load the lumbar and thoracic spine then 33% of the 1/10 is all that is left for the cervical spine and skull. This changes the calculations:

When we divide by 32.2 fps/s, we end up with 12.17 g’s at the cervical spine and skull. Notice this is almost exactly three times the initial 3.65 g’s at the hip.[2]

The graph below visualizes the forces experienced. The orange line is the force experienced at the cervical spine if twice the lumbar, the grey line is the force experienced at the cervical spine if three times the lumbar spine.

Now that we have explored the quantification of forces applied, let's look at how the forces act on humans. Below is a graph which depicts the forces experienced in everyday events as well as the collision we discussed earlier in this writing (8 mph at .1 seconds).

Consider how the forces on the bottom of the slide can act on a human, is coughing a natural act? Why is it then that the cited reference, (Brault et al 1998) can establish injury to the cervical spine and we can quantify that value at almost the same as coughing? By this comparison coughing and a rear-end collision at 2.49 mph should result in almost the same injury every time. Why then are doctors and hospitals everywhere not overrun with patients who have cervical spine injuries from coughing?

The answer is HOW the forces are applied to us! Walking, sneezing, coughing, hopping, sitting in a chair, etc. are actions we, as humans, are biomechanically designed to do. We do these things every day with no negative sequelae. However, when you sit in a vehicle and you are struck from behind nothing about that action mimics an activity which is normal to us. Being accelerated from behind in a short amount of time, such as a car collision, is not a natural action and not something we are designed to do.

When considering traumatic bodily injury to the human spine, advanced knowledge of spinal biomechanical engineering and spinal function at both the global and regional scale is a necessary requirement. Advanced knowledge is inclusive of the resistive forces of connective tissue attachments, bony stabilizing mechanisms and central nervous system (brain) innervation for both the guarding and the compensatory aspects of the body’s response to injury. Additional application of the principles of physics regarding the forces applied to the occupant in trauma, gives the provider a scientific rationale for causation and bodily injury devoid of false perception and rhetoric. The combination of spinal biomechanical engineering knowledge and an understanding of the physics of the forces applied will resolve most questions of fact and provides a demonstrable answer when assigning the cause of bodily injury.




  1. Siegmund, G. P., King, D. J., Lawrence, J. M., Wheeler, J. B., Brault, J. R., & Smith, T. A. (1997). Head/neck kinematic response of human subjects in low-speed rear-end collisions. SAE transactions, 3877-3905

       2. Brault J., Wheeler J., Gunter S., Brault E., (1998) Clinical Response of Human Subjects to Rear End Automobile Collisions, Archives of Physical Medicine and Rehabilitation, 79 (1) pgs. 72-80


[1] There is a change at the beginning and end of the maneuver, good for you if you recognized this!

Image Credit: Wikipedia Commons

[2] There are some variances in the results and the graphs, this is a prime example of rounding and/or truncating throughout the calculations.

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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.  


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Disc and Ligament Injuries: How Spinal Experts Document Causality    

By:  Johnston, J. Studin, M., (2016)

“The clinical presentation is a disc bulge in their neck and some arthritis, so their neck symptoms are not related to the crash. There is a low back herniation but lots of people have those and don’t have pain.  It is our opinion it was there before the crash.”  This statement from an adjuster is an argument that has been made for years allowing insurance companies to inappropriately reduce settlements to their clients based on the client’s inability to prove when or how their injury really occurred.  To factually counter this type of statement, one must use imaging and age dating with an understanding of biomechanics in order to demonstrably discuss causality. Without medical experts utilizing the current medical and academic research available, it will continue to be difficult for any argument to be made explaining the nature of and long-term effects of these injuries based on scientific fact vs. rhetoric

Imaging of the spine is critically important in all cases of injured clients.  In traumatic cases, imaging is necessary for diagnosis, triage and proper co-management of bodily injuries.  Imaging needs to be performed as per the current academic and contemporary medical/chiropractic standards to ensure an accurate diagnosis.  The most common injuries in car accidents are spinal related, and the basic imaging available includes x-rays, CAT scans and magnetic resonance imaging (MRI), allowing medical providers to make an accurate diagnosis, when clinically indicated. 

Every medical provider in Colorado (MD, DO, DC for diagnosis/prognosis purposes) has a license to see and treat car related injuries.  However a “license” is not the same as “specialization.”  By way of illustration, although psychiatrists are MDs and might have a license to do heart surgery, it would not be in the best interest of the patient.  Nor would I go to a spine surgeon for psychological concerns even though they are fully licensed to treat medical conditions.  In spinal trauma, certain providers specialize in connective tissue injuries of the spine, allowing us to go one step further in diagnosis, prognosis and management, including “age-dating” these commonly found disc and ligament injuries.

To understand age-dating, one needs to have a basic medical understanding of anatomy and physiology, as well as what tissue is commonly injured and the probable “pain generator”.  Since neck injuries are the most common injuries seen in car crashes, cervical spinal joints will be our focus. Related to anatomy, every set of two vertebrae in the neck is connected with three joints; one disc and two facet joints.  These joints allow for normal movement of the spine (mobility).  Additionally, there are multiple ligaments that hold these joints together and are responsible for stability.  The proper balance of mobility and stability is critical when looking at the biomechanical part of patient’s injuries, meaning that too much or too little movement in spinal joints can cause pain, secondary to damaged tissue.  The tissue most commonly injured in a car crash is muscle/tendon, ligament, disc, facet and nerve.  Spinal cord and bone injuries also occur although less frequently.  To determine causality, the provider should comment on what tissue is injured, and also use imaging to help determine when this injury occurred (age-dating).

There are two basic problems that must be addressed. Fardon 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).  Simply having the presence of a disc herniation, without a physical exam or without proper symptom documentation, does not allow one to comment on the cause of the injury.  In a rear impact collision for example, even when the diagnosis is confirmed, additional criteria need to be met to answer the question of “Was there enough force generated into the vehicle and the occupant to cause the cervical/lumbar herniation?” Fardon, in a follow-up study (2014) reported that disc injury “in the absence of significant imaging evidence of associated violent injury, should be classified as degeneration rather than trauma.” (p. 2531).  So, we must more objectively define the subjective connotations of “violent injury” and address the issue of “degeneration rather than trauma”. Although this statement can often be misleading, it gives the trauma trained expert doctor a basis in going forward understanding that every patient’s physiology is unique and not subject to rhetoric, but clinical findings.

Violentinjury to the occupant can occur when there are sudden acceleration and deceleration forces (g’s) generated to the head and neck that overwhelm connective tissue or bring them past their physiological limit.  To determine the acceleration force, ΔV (delta V) is used.  ΔV is the change in velocity of the occupant vehicle when it is hit from behind (i.e., going from a stopped position to seven miles per hour in 0.5 seconds due to forces transferred from the “bullet” vehicle to the “target” vehicle).  Using these data, research allows us to make specific comments related to violent injury. For the purpose of this article, we are oversimplifying because the cervical spine is exposed to compression, tension, and shearing forces. In addition to g-forces and the elastic nature of most rear impact crashes makes it nearly impossible to find a true minimum threshold for injury although the literature has given us many examples of low-speed crashes that are dependent not simply on speed, but the mass (weight) of the subject vehicles.  Each person’s susceptibility to injury is unique.  While g-forces alone are insufficient to predict injury, Krafft et al. (2002) reported that in low-speed collisions there is an injury threshold of 4.2 g’s for males and 3.6 g’s for females.  Krafft’s research is unique in that she has access to insurance data inaccessible to most researchers.  Panjabi (2004) showed that forces as low as 3.5g impacts would cause damage to the front of the disc, and 6.5g and 8g impacts would cause disc damage posteriorly where the neurological elements are.

A spinal biomechanical expert can then look for conclusive evidence by age-dating disc and joint pathology, based on two phenomena.  First, it is well known that the body is electric.  When an EMG is performed we are measuring electrical activity along nerves to diagnose radiculopathy, which is nerve damage.  Second, there are also normal bioelectrical fields in all tissue, known as piezoelectricity.  When an injury occurs, this normal electrical field is disrupted, and in the case of spinal joints calcium is drawn into the damaged tissue creating bone spurs.  Issacson 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).  Fortunately for the patient, we are able to tell how much of this process has occurred either before or after their crash, specifically when we take into account the soft tissue damage seen and evidence of bone/calcium deposition.

Additionally, the body begins a healing process that includes regeneration and remodeling of both soft and hard tissue as reported by Issacson and Bloebaum (2010).  Spinal vertebrae have a unique structure of bone that allows it to adapt to abnormal mobility and stability (injury) by changing shape, which can be seen on radiographs or MRI.  Furthermore, the bone will change shape according to predictable patterns based on the increased pressure or load that it undergoes post-injury. Issacson and Bloebaum stated that “Physical forces exerted on a bone alter bone architecture and is a well-established principle…” (p. 1271).  This is a further understanding of a scientific principle known as Wolff’s law, first established in the 1800’s.  Since we know what “normal” is, when we see “abnormal” findings due to mechanical stress we can broach the topic of an acute injury versus a degenerative process being the cause of the abnormality and make specific medical predictions accordingly.

He and Xinghua (2006) studied the predictability of this bone remodeling process and were able to make predictions of pathological changes that will occur in bone, specifically the osteophyte (bone spur) on the edge of a bone structure.  Significantly, they noted their findings “confirmed that osteophyte formation was an adaptive process in response to the change of mechanical environment”.  They noted that mechanical factors are crucial to the morphology of bones, notably load-bearing bones such as the femur and vertebrae. 

For readers familiar with current medical and academic accepted nomenclature for disc damage, recognized by the combined task forces of the North American Spine Society (NASS), the American Society of Spine Radiology (ASSR) and the American Society of Neuroradiology (ASNR), disc herniations must have a directional component. When this occurs, the abnormal and additional pressure at the level of the disc damage matched with the direction of the herniation will cause only that part of the vertebrae to remodel.

Thus, if there is a C5/6 right sided herniation (protrusion/extrusion) secondary to a cervical acceleration/deceleration injury, then only that side of the vertebrae will change shape, creating an osteophyte.  This compounded loading on the facet joint additionally causes facet arthritis.  This process is similar to the formation of a callous on your hand or foot.  The callous is a known and expected tissue response to increased load/friction exposure. Similarly, an osteophyte is a known and expected bone response to an increase in load/friction exposure.

At a basic level, the body has an electrical and mechanical response to injury resulting in additional stress that causes calcium (bone) to flow into the area of injury to further support the joint. The joint then abnormally grows, creating a pathology called hypertrophy, degeneration, disc osteophyte complex, or arthritis/arthropathy, common terms seen in radiology and doctor’s reports.           

Everyone is subject to these morphological (structural) changes, always and predictably dependent on 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 six months for an osteophyte (bone spur) to be demonstrable post-mechanical failure or imbalance. This again provides 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 six months old, dependent on location and direction of the pathology.

In conclusion, that by definition, a disc is a ligament connecting a bone to a bone and it has the structural responsibility to the vertebrae above and below to keep the spinal system in equilibrium. Damage to the disc due to a tear (herniation or annular fissure) or a bulge will create abnormal load-bearing forces at the injury site.  These present differently depending on [1] if traumatic, as biomechanical failure on the side of the disc lesion, or [2] if age related, as a general complex.  Since other research and human subject crash testing have defined the term “violent trauma” as not being dependent upon the amount of damage done to the vehicle but rather to the forces to which the head and neck are exposed, we can now accurately predict in a demonstrable manner the timing of causality of the disc lesion. This is 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 mere rhetoric or speculation.


  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. 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. 19th Int. Techn. Conf. on ESV, Paper No. 05-0363, 1-7
  4. Batterman, S.D., Batterman, S.C. (2002). Delta-V, Spinal Trauma, and the Myth of the Minimal Damage Accident. Journal of Whiplash & Related Disorders, 1:1, 41-64.
  5. Panjabi, M.M. et al. (2004). Injury Mechanisms of the Cervical Intervertebral Disc During Simulated Whiplash. Spine 29 (11): 1217-25.
  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. Studin, M., Peyster R., Owens W., Sundby P. (2016) Age dating disc injury: Herniations and bulges, Causally Relating Traumatic Discs.
  8. 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.
  9. 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.

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  Pressure, Stopping Distance and Causality - Part II


By: Patrick Sundby, Accident Investigator

Specializing in Low Speed and Catastrophic Crashes



In the previous writing we created the foundation of the importance of tire pressures.  Specifically, we demonstrated a third of the vehicles on the road have an underinflated tire and further only a third of those vehicles have a warning light. 

We also know a 20% reduction in pressure results in substandard performance, these are the factors we are going to explore. 

Underinflated tires have a different profile and contact patch with the road surface. 

Where the tire meets the roadway is referred to as the contact patch.  Maximizing the contact patch affords the driver the most performance, specifically steering and braking.  What happens when we reduce the contact patch?  Under inflation does just that.

The contact patch is what connects the vehicle to road, when a tire is properly inflated (all other factors being ignored), the tire can give 100% of the contact patch (and the friction between the tire and the roadway) to steering, braking or a combination of both.  If the pressure drops the contact patch is reduced and thus performance is also reduced - but by how much?  There are varying schools of thought on this and a ton of research, for our discussion we will say underinflated tires will have a reduction in performance by 15% across all categories. 

But what does this really mean in the real world?  Let say a vehicle traveling at 20 mph with properly inflated tires had to swerve to avoid a collision and was successful.  This same vehicle with underinflated tires could successfully avoid the same collision at no more than 17 mph.  Let’s increase the speeds, 55 mph properly inflated collision avoidance becomes 48 mph underinflated collision avoidance.

How about braking?  If a vehicle with properly inflated tires could stop in 200 feet (approximately 70 mph), the same vehicle with under inflated tires would need 230 feet.

Rollovers become another related concern.   Besides the contact patch, proper inflation also affects sidewall rigidity and stability.  In simple terms as a tire is asked to change direction (steer), an underinflated tire will flex enough to allow the sidewall touch the roadway surface and lift the contact patch from the roadway.  In extreme cases, the tire will separate from the rim allowing the rim to dig into the roadway surface.  The photo below depicts a sidewall which is experiencing this condition.

Photo credit: corvetteforms.com

The tires in this photo are still able to perform well, in part due to the very small side wall and lack of extreme under pressures.  Increasing the sidewall, similar to a truck or SUV, magnifies the flex and distortion.

The final point to touch on is the increase of blowouts.  Underinflated tires put stress on the tire structure and increase heat inside the tire.  These factors can, and do, increase the odds of a tire failure by inducing or exacerbating the layers of material within the tire to separate.

Proper tire inflation is one of the single most important routine maintenance task, and ironically, one of the most ignored tasks and when considering causality, the tire pressure should be checked to help reconstruct the entire picture of the accident. Tire pressure should also be considered when determining braking distances and skid marks and is often the arbiter of the culpable party.

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 had the privilege of participating in both learning and teaching 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 level. He can be reached at 571-265-8076 or patrick.sundby@gmail.com

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 postdoctoral education, teaching MRI spine interpretation and triaging trauma cases. He is also the president of the Academy of Chiropractic, teaching doctors how to interface with the legal community (www.DoctorsPIProgram.com). He teaches MRI interpretation and triaging trauma cases to doctors of all disciplines nationally, and studies trends in health care on a national scale (www.TeachDoctors.com). He can be reached at DrMark@AcademyofChiropractic.com or at 631-786-4253.


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Soft Tissue Injuries

What are they and the Long-Term Impact of Bodily Injury




According to the American Academy of Orthopedic Surgery “The most common soft tissues injured are muscles, tendons, and ligaments. Acute injuries are caused by a sudden trauma, such as a fall, twist, or blow to the body. Examples of an acute injury include sprains, strains, and contusions.”  (http://orthoinfo.aaos.org/topic.cfm?topic=A00111) We must also not forget that there are other soft tissues that can get injured and the true definition of soft tissue, which is anything not bone is soft tissue. This includes the brain, lungs, heart and any other organ in the body. However, in medicine soft tissue injuries are commonly known to be limited to the muscles, ligaments and tendons. 

When we look at the type of structures that muscles, tendons and ligament are composed of, we will realize that they are connective tissue. According to the National Institute of Health “Connective tissue is the material inside your body that supports many of its parts. It is the "cellular glue" that gives your tissues their shape and helps keep them strong. It also helps some of your tissues do their work (http://www.nlm.nih.gov/medlineplus/connectivetissuedisorders.html). Unlike fracture repair where the bone is replaced and usually heals properly if aligned and rested, connective tissue disorders undergo a different type of wound repair that has aberrant tissue replacement as sequella to bodily injury and has subsequent abnormal permanent function.

If we focus on sprains or ligamentous injuries, according to the American Academy of Orthopedic Surgery there are three types of sprains:

Sprains are classified by severity:1

  • Grade 1 sprain (mild): Slight stretching and some damage to the fibers (fibrils) of the ligament.
  • Grade 2 sprain (moderate): Partial tearing of the ligament. There is abnormal looseness (laxity) in the joint when it is moved in certain ways.
  • Grade 3 sprain (severe): Complete tear of the ligament. This causes significant instability and makes the joint nonfunctional.

Regardless of the severity of the sprain, there is tissue damage or bodily injury and the next step is to determine if there is healing or wound repair. According to Woo, Hildebrand, Watanabe, Fenwick, Papageorgiou and Wang (1999) “…as a result the combination of cell therapy with growth factor therapy may offer new avenues to improve the healing of ligament and tendon. Of course, specific recommendations regarding growth factor selection, and timing and method of application cannot be made at this time. Previous attempts at determining optimal doses of growth factors have provided contradictory results. Although growth factor treatment has been shown to improve the properties of healing ligaments and tendons, these properties do not reach the level of the uninjured tissue.” (p. s320)

According to Dozer and Dupree (2005) “No treatment currently exists to restore an injured tendon or ligament to its normal condition.” (pg. 231).

According to Hauser, Dolan, Phillips, Newlin, Moore and Woldin (2013) “injured ligament structure is replaced with tissue that is grossly, histologically, biochemically and biomechanically similar to scar tissue. Fully remodeled scar tissue remains grossly, microscopically and functionally different from normal tissues” (p. 6) “the persisting abnormalities present in the remodeled ligament matrix can have profound implications on joint biomechanics, depending on the functional demands placed on the tissue. Since remodel ligament tissue is morphologically and mechanically inferior to normal ligament tissue, ligament laxity results, causing functional disability of the affected joints and predisposing other soft tissues in and around the joints further damage.” (p.7) “studies of healing ligaments have consistently shown that certain ligaments do not heal independently following rupture, and those that didn’t feel, do so characteristically inferior compositional properties compared with normal tissue. It is not uncommon for more than one ligament undergo injury during a single traumatic event.” (p.8) “osteoarthritis for joint degeneration is one of the most common consequences of ligament laxity. Traditionally, the pathophysiology of osteoarthritis was thought to be due of aging and wear and tear on the joint, but more recent studies have shown that ligaments play a critical role in the development of osteoarthritis. Osteoarthritis begins when one or more of ligaments become unstable or lax, and the bones began to track improperly and put pressure on different areas, resulting in the rubbing the bone on cartilage. This causes breakdown of cartilage and ultimately leads to deterioration, whereby the joint is reduced to bone on bone, a mechanical problem of the joint that leads to abnormality of the joints mechanics. Hypomobility and ligament laxity have become clear risk factors for the prevalence of osteoarthritis.” (p.9)

Looking globally at the research over the last 16 years, in 1999 it was concluded that the most current treatments to repair or heal the injured ligament do not reach the level of the uninjured tissue. In in 2005 it was concluded that no treatment currently exists to restore an injured tendons or ligaments to its normal condition. In addition the current standard of ligament research in 2013 concluded that that ligaments do not feel independently, but damage ligaments are a direct cause of osteoarthritis and biomechanical dysfunction (abnormality of joint mechanics). The latest research has also concluded that ligament damage or sprains is the key element in osteoarthritis and not simply aging or wear and tear on the joint.

As a result it is now clear based upon the scientific evidence that a soft tissue injury is a connective tissue disorder that has permanent negative sequela and is the cause of future arthritis. This is no longer a debatable issue and those in the medical legal forum who are still arguing “transient soft tissue injuries” are simply rendering rhetoric out of ignorance and a possible ulterior motive because the facts clearly delineate the negative sequella based upon decades of multiple scientific conclusions.

The caveat to this argument is that although there is irrefutable bodily injury with clear permanent sequella, does it also cause permanent functional loss in every scenario? Those are two separate issues and as a result of the function of ligaments, which is to connect bones to bones the arbiter for normal vs. abnormal function is ranges of motion of the joint. That can be accomplished by either a two-piece inclinometer for the spine, which according to the American Medical Association Guides to the Evaluation of Permanent Impairment, 5th Edition (p. 400) is the standard (and is still the medical standard as the 6th Edition refers to the 5th for Ranges of motion). The other diagnostic demonstrable evidence to conclude aberrant function is to conclude laxity of ligaments through x-ray digitizing. Both diagnostic tools confirm demonstrably loss of function of the spinal joints.   


  1. Sprains, Strains and Other Soft Tissue Injuries (2015) American Academy of Orthopedic Surgery, Retrieved from: http://orthoinfo.aaos.org/topic.cfm?topic=A00111
  2. Connective Tissue Disorders (2015) National Institute of Health, Retrieved from: http://www.nlm.nih.gov/medlineplus/connectivetissuedisorders.html
  3. Woo S, Hildebrand K., Watanabe N., Fenwick J., Papageorgiou C., Wang J. (1999) Tissue Engineering of Ligament and Tendon Healing, Clinical Orthopedics and Related Research 367S pgs. S312-S323
  4. Tozer S., Duprez D. (2005) Tendon and Ligament: Development, Repair and Disease, Birth Defects Research (part C) 75:226-236
  5. Hauser R., Dolan E., Phillips H., Newlin A., Moore R. and B. Woldin (2013)  Ligament Injury and Healing: A Review of Current Clinical Diagnostics and Therapeutics, The Open Rehabilitation Journal (6) 1-20
  6. Cocchiarella L., Anderson G., (2001) Guides to the Evaluation of Permanent Impairment, 5th Edition, Chicago IL, AMA Press

Note about the author: Dr. Mark Studin teaches at the doctoral level as an Adjunct Assistant Professor of Chiropractic at the University of Bridgeport, College of Chiropractic, and an Adjunct Assistant Professor of Clinical Sciences at Texas Chiropractic College. He also teaches at the graduate medical level as a clinical presenter credentialed by the Accreditation Council for Continuing Medical Education in Joint Sponsorship with the State University of New York at Buffalo, School of Medicine and Biomedical Sciences along with being credentialed nationally for chiropractic post-doctoral education in a broad range of clinical subjects. Dr. Studin’s CV can be accessed by CLICKING HERE

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