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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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. (


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:(
  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 (, teaches MRI interpretation and triaging trauma cases to doctors of all disciplines nationally and studies trends in healthcare on a national scale ( He can be reached at 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 or or 716-228-3847  

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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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