Injury Care Chiropractic - Louisville Chiropractor

                       Personal Injury Report 

          Dr. Harold Byers, Jr., B.A., M.S., D.C.


One of the most important parts of a personal injury case is finding the doctor/s who are experienced in these type cases.  Dr. Byers, Jr., M.S., D.C. has seen over 30,000 injuries and given over a million treatments.  He is one of the most experienced doctors in the United States and knows how to treat those who are suffering with accident pain.  Consultations are always free and you can call Injury Care Chiropractic at 502-635-2273.

        Analyzing Injuries Sustained In Low-Speed Car Crashes

The managing director of GBB Ltd Forensic Collision Investigation and Research, Brian Henderson discussed results reveals the results of his extensive research into the impact of low-speed-change collisions.

It is often claimed that below a certain speed change “injury will not occur,” and this threshold is purported to be 5 mph.        
Collisions between motor vehicles and the occupants of those vehicles must conform to Newton’s Laws of Motion.

The mathematical principles of collision physics are complex and unique for each accident.  Yet, they can be simplified, as many of the forces involved are so small that for practical purposes they are negligible.  Importantly, these principles often support the position of the patient and their doctor.

Sir Isaac Newton at the age of 43 published the book Principia Mathematic, which is among the most influential books in the history of science.  In Principia Mathematic, Newton describes the three Laws of Motion.  

It is Newton’s Law of Motion that explains contemporary whiplash trauma and subsequent injury.  The most important Law is his first, the Law of Inertia.  Simply stated in the context of Whiplash trauma, things at rest tend to remain at rest, and different parts of the same object can have different inertias.

The human body has two large parts that have their own separate inertia, the trunk and the head.  These two large pieces of inertia mass (the head and the trunk) are connected by the thinner structure of the cervical spine.  During a motor vehicle collision, a vehicle that is struck from behind will quickly move forward.  As the vehicle moves forward, so does the passenger seat in the vehicle.  As the passenger seat moves forward, so does the trunk of the passenger sitting in the seat.  However, the head of the passenger in the seat does not move forward because the head has a separate inertia from the trunk.  As the vehicle, the seat, and the trunk move forward from the collision, the head remains at rest, forcing the neck backwards.  The result is an inertial injury to the soft tissues of the vertebral joints of the cervical spine.  Importantly, the neck does not hit anything; it sustains an inertial injury, similar to that seen in shaken baby syndrome.

It is important to consider what occurs to the cervical spine during this instantaneous event.  Ono et. al. provided some of the best information pertaining to biomechanics of the spine in the image below, the four phases of the s-shaped curve.
The s-shaped curve, with hyperextension of the lower segments and flexion of the upper segments. This is one of the chief points of injury and occurs before the head strikes the head restraint.  Adapted from Ono et al.   

      “Historically, the argument about injury or likelihood of injury had been the domain of the medical experts, albeit without any true scientific evidence on which to base an opinion.” 

A struck vehicle will accelerate forward, with or without vehicle damage. This
will cause accelerations of the occupant’s chest and head.

Brian Henderson and his colleagues have produced crashes resulting in a change in velocity of 5.97 mph of the struck vehicle. This caused a 4.7 g acceleration of the occupant’s chest and an 8.3 g acceleration of the occupant’s head. The difference between the head and chest acceleration was 3.6 g. This resulted in the symptoms of strains and headaches.      
This author and his colleagues have also produced collisions that produced a change in velocity between 2.8 to 3.1 mph. This resulted in a chest acceleration of 2.93 g and a head acceleration of 3.46 g.  The difference between the chest and head acceleration was 0.53 g.
However, this research also showed that not all occupants reacted in the same manner to the same change in velocity.

Brian Henderson states:
1) “It is my opinion that beyond a speed change of 5 mph, the risk of injury is high.”
2) “The risk [of injury] between 3 mph and 5 mph [speed change] is a grey area that would need further exploration, and injury cannot be ruled out.”
3) “The risk [of injury] below 3 mph [speed change] is minimal”.
From this research, we can effectively reconstruct an accurate sequence of events in a typical Low Speed Rear Impact Collision (LOSRIC), without the cumbersome and tedious citing of specific references. The following is thus a composite of all of the relevant literature, relying heavily on the work of Ono et al. and Siegmund et al., as well as research from the Spine Research Institute of San Diego crash testing data. 

Bear in mind, of course, that special risk variables can significantly alter the kinematic response to cervical acceleration / deceleration (CAD) trauma. These studies are based on an ideally positioned occupant, in a relatively good state of health, looking straight forward, wearing restraint belts, using a head restraint, and seated in a standard car seat and in a car struck squarely from the rear (180 degrees) with good bumper alignment (i.e., no over-ride or under-ride, and no offset), and free runout (i.e., no second collisions). The model is also applicable to speed changes of about 2.5 mph to 6 mph. I'll refer to this model as the Ideal Low Speed Rear Impact Collision (LOSRIC) Model. Later, we'll discuss specific known risk factors which can be used to refine our understanding of the kinematic responses of specific (i.e., atypical) crashes.
Upon impact, the target vehicle begins to move forward into the occupant, making contact chiefly through the seat back. In accordance with Newton's 1st law of motion, the occupant's inertia resists this motion. 

As the seat back continues to move forward, the occupant must yield. Initially, the thoracic curve is flattened by the seat back. This results in a vertical compressive force which is transmitted through the spine. 
So far, we have not been able to determine to what degree--if any--the lumbar spine also flattens. As the vertical compressive force (-z) continues up the spine, some rise of the torso also occurs. This is called ramping and is halted after 1-3 inches of vertical displacement, usually because of  the restraining effect of the seat belt and the weight of the torso. Meanwhile, as the torso now is undergoing both a “z” acceleration vertical and an “x” linear acceleration, the head--also acting in accordance with Newton's 1st law of motion--attempts to remain at rest. As the vertical force extends upwards into the neck, it initiates flexion of the upper cervical segments and hyperextension of the lower segments. Compression then quickly gives way to tension as the upward moving head and now downward moving torso attempt to disengage. 

Also, as the torso moves forward with respect to the head, significant amounts of horizontal shear force occur in the neck roughly parallel to the facet joint line. As this is initiated under conditions of compression, the overall stiffness of the neck may be diminished as a result of ligamentous slack as we will discuss, offering less resistance to shear.
As the torso continues to move forward, the neck begins to pull the head along with it. This has the effect of further flexing the upper cervical spine and hyperextending the lower cervical spine (primarily the C5-6 segments) and the spine assumes an s-shaped configuration, as seen in the above diagram. The head also is induced to extend along with the neck as the head takes up the backset distance during the head lag phase. 

Depending on specific head restraint geometry (occupant's position relative to the restraint), head restraint contact will usually occur in about 100 msec at which time head translational acceleration will peak. 

Any stored energy in the seat back from its deflection (usually about 5-15 degrees) will be released as the occupant begins to more forward into the re-entry phase. This effectively increases the torso and head speed (overspeed).

                                 Structural Integrity Injuries
Anterior Longitudinal Ligament Injury During Whiplash
A number of recent studies have begun to examine the issue of ligament damage after whiplash. The intervertebral ligaments are the key to spinal stability; if they are stretched or torn during a car crash, a myriad of symptoms can result.

A current study was conducted using 6 fresh-frozen whole cervical spine (WCS) specimens: 4 specimens were male and 2 were female, with an average age of 70.8 years. The specimens were mounted top and bottom in a neutral position at the beginning of the study, and lightweight motion-tracking flags were inserted into the anterior (front) aspect of each vertebra (C2-C7) to allow better angle calculations.

Rear-impact whiplash trauma was simulated using a bench-top sled apparatus, with the trauma applied successively at 3.5 g, 5 g, 6.5 g and 8 g, after an initial 2 g preconditioning run. Spinal motion during the impact was measured using high-speed digital cameras (with recording conducted at 500 frames per second).

Initial spinal x-rays were recorded and digitally scanned in the neutral position. Motion-tracking software was then used to track the intervertebral rotations and the motion of the individual vertebral segments during the testing/trauma application. Graphs were created of the movement of each of the cervical vertebrae (C2-C7) during the impact trials.

The strain to each anterior longitudinal ligament (ALL) was calculated by dividing the increase of ALL length during impact by the original ALL length, expressed as a percentile.
ALL strain was defined as the peak extension at trauma, minus the normal physiologic value determined before testing. Visual inspection was also done after the 8 g trauma, and ALL injury was classified into one of 3 groups:

• Class 0: No visible (macroscopic) injury
• Class I: Partial injury with no visible injury to the underlying annulus
• Class II: Complete injury with underlying annulus involvement

The average ALL length was 13.3 mm in the neutral position. During trauma, the ALL tended to elongate with head extension, then returned to its original length when the head returned to a neutral position. Significant increases in ALL strain (beyond normal physiologic movement) was first seen at 3.5 g of trauma at the C4-C5 level; this observed strain increased to include C5-C6 at 5 g of trauma, and included C6-C7 at 6.5 g. A trend towards strain was seen at C3-C4 at 8 g of trauma. Peak ALL strains were largest in the lower cervical spine at all levels of trauma and increased with impact acceleration, with an average peak strain of 29.3% at 8 g.

During visual inspection of the 30 ALL specimens:
• 4 sustained class I injuries
• 6 sustained class II injuries
• 20 were uninjured (class 0)

The anterior longitudinal ligament runs along the front of the spine, and plays a critical role in spinal stability.


                           Anterior Longitudinal Ligament

ALL extension and strain was significantly greater in the class II group than in the class 0 group, with the average class II ligament length increase (39.2%) nearly double that of the class 0 group (17.5%). Class I and class II showed similar strain patterns, with the tendency towards strain greater for class II.

This study showed that the greatest anterior longitudinal ligament (ALL) strains occur in the lower cervical spine during simulated whiplash injury, and that strain severity increases with the severity of impact. The ALLs located at the middle and lower cervical spine (C3 and C7) appeared to be at the greatest risk of strain/injury in impacts greater than 3.5 g.

The ALL strain and intervertebral extension was greater in class II injuries than in class 0, suggesting that greater levels of intervertebral extension are associated with an increased risk of ALL strain and higher injury potential.

Both normal zone and ROM increased significantly with class II injuries, demonstrating measurable cervical instability with increasingly severe injury.

The study authors note that the study results compare favorably with clinical evidence, with several previous studies noting C5-C7 ALL and anterior annulus damage in patients with severe whiplash documented with MRI, or by visual inspection during surgery or post-mortem. It appears that whiplash injuries and resulting ALL injury are first seen in the lower cervical spine; then, with greater impact, the injury moves up to the mid-cervical spine.

The class II injuries seen during the study also indicated that a small portion of the population may be at risk for complete ALL tears during whiplash injury. It also showed that there is a loss of cervical stability when the anterior stabilizing system is disrupted, and could be one cause of chronic pain after whiplash injury. Injury to these anterior soft tissues could also lead to increased loading and degeneration of the posterior spinal components, and contribute to the facet joint pain seen in some whiplash patients with chronic pain.

                      Angular Acceleration And Head Injuries
The mechanism of the trauma was previously thought to be a shearing of axons which result from abrupt acceleration and deceleration of brain tissue. During a low speed whiplash injury (7 mph) the head may be accelerated to 9-18 g. Since the brain is a soft structure, shear strains are created as the outer part of the brain moves at a different pace than the inner part of the brain. This is intensified as the momentum of the head changes rapidly in a sagittal direction during a whiplash trauma.
Ommaya AK, Gennarelli TA: Cerebral concussion and traumatic unconsciousness.  Brain 97:6330654, 1974.
West DH, Gough JP, Harper TK: Low speed collision testing using human subjects. Accid Reconstr J 5(3):22-26, 1993.

There is no doubt that individuals involved in minimum structural damage collisions develop symptomatology consistent with whiplash type neck distortion connective tissue injuries.  Practicing health care providers who examine these patients document findings that are consistent with soft tissue trauma.  
These include:  
  • Alterations of segmental motion 
  • Alterations of joint end play
  • Postural distortions 
  • Alterations of normal tissue textures 
  • Abnormal sensitivity (pain) to local pressure 
  • Swelling
In addition, more expensive diagnostic investigations often show alterations of segmental motion with clinical tools such as;  
  • Stress radiography flexion / extension and lateral flexion open mouth studies   
  • Stress MRI flexion / extension, lateral flexion and upper cervical studies
  • Inflammatory changes consistent with soft tissue injury 
  • Thermography 
  • Abnormal neurological function with surface EMG 
  • Objectively measured reduced pain thresholds with algometry 
  • Objective alterations of global range of spinal motion with dual inclinometers

Rear impact motor vehicle collisions are also classified as “inertial acceleration injuries.” Popular terminology within our profession is “cervical acceleration / deceleration syndrome,” or CAD (Foreman and Croft).  These inertial acceleration injuries to the cervical spine are proportional to the acceleration achieved by the struck vehicle.  
The greater the acceleration of the struck vehicle, the greater the acceleration injuries to the cervical spine structures.  Importantly, sufficient vehicle acceleration to cause cervical spine inertial acceleration injuries can occur with no or minimal vehicle structural damage.  This concept is adequately explained by Robbins (Journal of the Society of Automotive Engineers, 1997) and others, below.  

Robbins article is titled: 
Lack of relationship between vehicle damage and occupant injury

We have provided this example in earlier PII newsletter in the past but it is worth repeating.  In agreement with above, Robbins states that injury is linked to the magnitude of the acceleration achieved by the struck vehicle.  
Acceleration is expressed in the units of “G” which stands for the acceleration of gravity.  Falling in gravity is not a velocity (a steady speed); it is an acceleration (going faster every second).  1G = 9.81 meters/second² (m/s²).  Robbins states the pertinent mathematical formula is from the great Italian physicist, mathematician, and astronomer, Galileo (d. 1642) :
A = V²/2s
a = acceleration
V = velocity of impact
S = the crush distance of the vehicle
Using Galileo’s mathematical formula, Robbins cites two examples:

Look at the numbers carefully.  In the second example, for the same velocity, crushing the vehicle 80% less (1 meter versus .2 meters) resulted in significant more vehicle acceleration (5 times more [7 Gs v. 36 Gs]).  The results show that the greater the crush damage distance of the vehicle, the less the G force received by the occupant.  Or, the smaller the crush damage distance of the vehicle, the greater the G force received by the occupant, which is associated with greater acceleration inertial injury.
The use of stiff motor vehicle bodies and chassis, when subjected to relatively severe impacts, may result in little or no damage to the vehicle body or bumper, yet the occupants are subjected to high G force, resulting in whiplash injury. 

 Robbins states:
“….crush damage does not relate to the expected occupant injury, i.e., the more vehicle damage, the greater the chance that the occupant is injured, is not a conclusion that can be made.  In fact, it is more likely the opposite.”
Studies clearly indicate that motor vehicles can withstand a reasonably high-speed impact with little or no accompanying vehicle damage (Navin).  Unfortunately, when vehicle damage energy is reduced, the energy is transferred into acceleration, causing patient injury.  Current bumper standards have the effect of reducing property damage while subjecting the probability of occupant injury (Navin, Smith).
Published experts in motor vehicle collisions have completed experiments (Navin, Emori) or made observations which conclude that the degree of patient/passenger injury from automobile collisions is not related to the size, speed, or magnitude of damage of the involved vehicles.  

Navin and Romilly state (1989):
“….experimental results indicate that some vehicles can withstand a reasonable high speed impact without significant structural damage.  The resulting occupant motions are marked by a lag interval, followed by a potentially dangerous acceleration up to speeds greater that of the vehicle.
A review of accident reports indicates that a significant percentage occur with little or no accompanying vehicle damage.
As the vehicle becomes stiffer, the vehicle damage costs are reduced as less permanent deformation takes place.  However, the occupant experiences a more violent ride which increases the potential for injury.
…the average acceleration experienced by the occupant in the elastic [no damage] vehicle would be approximately twice that of the plastic [structurally damaged] vehicle.  This theory implies that vehicles which do not sustain damage in low speed impacts can produce correspondingly higher dynamic loadings on their occupants than those which plastically deform under the same or more severe impact conditions.”

Emori and Horiguchi state (1990):
“…neck extension became almost 60° which is the potential danger limit of whiplash, at collision speed as low as 2.5 km/h.”

Robbins notes (1997) that it is false reasoning and a misconception to claim that vehicle crash damage offers a correlation to the degree of occupant injury.  He states:
“This false reasoning is often applied by insurance adjusters, attorneys and physicians and frequently results in costly unjustified litigation.  Due to this litigation process, the injured parties often are not compensated, resulting in unjustified hardship to the party who has already been injured.”

Historically, a number of authors have made the observation that vehicle damage is not an indicator of occupant injury.  In 1964, physician and whiplash expert/author Ruth Jackson, MD, wrote:
“The forces which are imposed on the cervical spines of the passengers of colliding vehicles are tremendous, and if one attempts to calculate mathematically the amount of such forces, the results are unbelievable.”  
“The damage to the vehicles involved in collisions is no indication of the extent of the injuries imposed on the passengers.”  
“The extent of damage to the vehicles is in no way proportional to the extent of damage imposed upon the cervical spines of the passengers.”

Ian Macnab, MD, states (1982):
“The amount of damage sustained by the car bears little relationship to the force applied.  To take an extreme example: If the car was stuck in concrete, the damage sustained might be very great but the occupants would not be injured because the car could not move forward, whereas, on ice, the damage to the car could be slight but the injuries sustained might be severe because of the rapid acceleration permitted.”

Carroll et. Al. state (1986):
The amount of damage to the automobile bears little relationship to the force applied to the cervical spine of the occupants.  The acceleration of the occupant’s head depends upon the force impaired, the moment of inertia of the struck vehicle, and the amount of collapse of force dissemination by the crumpling of the vehicle.

Author Ameis, MD, states (1986):
“Each accident must be analyzed in its own right.  Auto speed and damage are not reliable parameters.”

Hirsch et. al. state (1988):
“The amount of damage to the automobile may bear little relationship to the forces applied to the cervical spine and to the injury sustained by the cervical spine.”

Smith states (1993):
“The absence of presence of vehicle damage is not a reliable indicator of injury potential in rear impacts.  Based upon the principle of conservation of energy, any energy which does not go into damaging the vehicle must be converted into kinetic energy, the source of injuries.”

Nordhoff and Emori state (1996):
“Historically, insurance company claims adjusters have assumed that collision injuries correlate to the vehicle external structural damage and cost repair.   …   The assumption that injuries relate to the amount of external vehicle damage in all types of crashes has no scientific basis.”
“There is little correlation between neck injury and vehicle damage in the low-speed rear-end collision.”

Rene Cailliet, MD, states (2006):  
“Simulated impacts have been studied extensively and essentially confirm that a low-speed impact with minimal or no damage to the impacted vehicle can and does cause significant musculoskeletal injury to the driver’s or occupant’s head and neck.”
“It has been shown that high speeds are not specifically pertinent in determining the extent of the [whiplash] injuries sustained.”
Numerous injuries result from vehicular accidents even when the impacts are not very big and there is minimal damage to both vehicles.”
“In many instances, a person experiences whiplash after a vehicle accident that has caused little significant damage to either vehicle.”

Importantly, published studies have reviewed both the presenting and long-term clinical status of consecutive patients’ injures in motor vehicle collisions.  Their conclusions support the mathematical principles of collision physics, the experimental studies of staged collisions, and the observations of published experts.  Specifically, Parmar and Raymakers (1993) reviewed 100 patients who had injured their necks in rear impact road traffic accidents.  They state:
There was no relationship between the prognosis and the type of car or the severity of damage it sustained.
“Some factors bare no relationship to the prognosis and they included…the amount of damage sustained by the vehicle.”  

Sturzenegger et. al. (1994) reviewed 137 consecutive patients after whiplash injury.  Their study specifically excluded patients with fractures, dislocations, head trauma, and preexisting neurological disorders.  The article states:
“The amount of damage to the automobile and the speed of the cars involved in the collision bear little relationship to the injury sustained by the cervical spine.”
…the velocities of the involved vehicles and the extent of car damage are not directly related to the forces acting on the cervical spine.”

Ryan et. al. (1994) reviewed 29 individuals who sustained a neck strain as a result of a car crash, and followed them for a period of six months.  They concluded:
“No statistically significant associations between crash severity and 6-month injury status were found. 
…there were no statistically significant relationships between injury status at 6 months and either measure of crash severity.
…there were no statistically significant associations between crash severity variables and injury status at 6 months…”

Sturzenegger et. al. in another published study (1995), 117 consecutive whiplash patients were followed for more than 12 months.  Again the authors state:
“Attempts to correlate outcome with extent of damage to the involved cars and their speed has previously been shown to be of little prognostic value.”

In 2002, accident reconstructionists Batterman and Batterman published research that concludes that no damage and low damage collisions do indeed produce forces that are injurious.  They note that literature which proclaims one cannot sustain whiplash injury in low speed accidents is scientifically and methodologically flawed and invalid.  They state:
“The results rigorously show that in a no damage accident the struck, or target vehicle can obtain a delta-v of 10 MPH or greater, which is well into an injury producing range.”

In 2004, Duffy and colleagues presented a case of disability following a bumper car collision.  The patient suffered debilitating, chronic neck pain after a low–velocity bumper car collision, with negative MRI, CT scan, and electromyography.  They state:
“A variety of factors, including the occupant’s awareness or head position in a colliding vehicle, defines the risk of neck injury to passengers in colliding vehicles.  One can only conclude that the threshold of injury is a complex dynamic relying on velocity, force, head position, head-torso angles, restraint placement, anticipation, tissue elasticity, tissue strength, and any multitude of variables that evade accurate determination.”
“The myriad of dynamic variables between occupant and vehicle precludes a definition of change-in-velocity thresholds for neck injury from car collisions.”
“Considering the complex mechanism of trauma, a common pathophysiology is not likely among all individuals with WAD, and their condition must therefore be assessed individually in light of the clinical syndrome and the objective findings.”
“This case history illustrates that a low-velocity collision can cause soft-tissue damage in the posterior neck, which may lead to chronic symptoms consistent with whiplash associated disorders.”

In 2005, Gun and colleagues prospectively followed 135 whiplash-injured patients for 1 year.  They concluded:
“Disability appears unrelated to the severity of the collision.”
“The degree of damage to the vehicle was not a predictor of outcome.”

Also in 2005, Pobereskin followed 503 whiplash-injured patients prospectively for 1 year.  Some of his comments include:
“Striking vehicle speeds are not related to initial neck VAS scores.”
“Striking vehicle speeds are not related to the number of days the victim will have neck pain.”
“Striking vehicle speeds are not related to neck pain severity initially or at one year or neck VAS scores at one year.”
“There is little evidence that the severity of the impact predicts the early onset of neck pain or pain at 1 year.”
“It is surprising that it has not been possible to relate estimated striking speeds to early whiplash or to any measure of neck pain severity either early on or at 1 year.”
In this study, driving a large car and being struck increased the risk of neck pain.  This “seems counterintuitive.”  “Large cars are less likely to deform and therefore more of the energy of the collision was transmitted to the occupants.”

The question arises then, why do occupants involved in seemingly small collisions have such significant symptoms and poor prognosis?  Part of the answer is because vehicles that crush less, accelerate more, and subsequent occupant injury is increased, as explained above.  McConnell et. al. (1995) analyzed the head and neck kinematics of 18 human volunteers subjected to rear impacts between 3.6 – 6.8 mph.  All volunteers were male of apparently good health, and they were “aware” of the fact that they were to be in a rear impact collision.  All test subjects reported some test related awareness or discomfort symptoms.  The tangential acceleration was found to typically reach values exceeding 10 Gs during the period up to 150 msec after the impact.  Yet, vehicle damage was minimal.
A second part of the answer concerns itself with the specific moment of impact biomechanics of the vehicle occupant.  Historically, authors have published an empirical association between whiplash type neck injuries and patient awareness prior to impact, and position of patient’s head prior to impact.  Importantly, research by Sturzenegger et. al. (1994), Ryan et. al. (1994), and Sturzenegger et. al. (1995) substantiates the empirical historical perspective that occupant awareness and head position are significant factors in injury and prognoses.

                                  Risk Factors (Awareness & Head Position)  

                           Awareness Factors
With respect to awareness,
  Emori and Horiguchi state (1990):
“If the passenger is aware of and anticipates a collision, and makes his neck muscle tense, he can tolerate more severe impact.”

Teasell and McCain state (1992):
“Injury results because the neck is unable to adequately compensate for the rapidity of head and torso movement resulting from the acceleration forces generated at the time of impact.  This is particularly true when the impact is unexpected and the victim is unable to brace for it.”

Smith states (1993):
“Research has shown that an occupant aware of an impending impact may progress sufficient muscle control to prevent hyperflexion and hyperextension during low velocity impacts.

Lord states (1993):
“In a whiplash injury, the acceleration-deceleration movements of the neck are typically completed within 250 msec.  The brevity of this period precludes any voluntary or reflex muscle response that might arrest, limit, or control the movements of a cervical motion segment.  Without muscle control the normal arcuate movement of a cervical must be disturbed, and the forces to which individual segments are subjected can be resisted only by passive ligamentous elements or bony contact.  This sets the scene for a variety of possible injuries.”

Teasell (1993) states that injury is greater;
“…when the impact is unexpected and the victim is unable to brace.”

Research by Ryan et. al. (1994) states:
“…awareness appears to have a strong prospective influence and may prove to be a useful prognostic indicator in clinical settings.
…subjects who were unaware of the impending collision had a greatly increased likelihood of experiencing persistent symptoms and/or signs of neck strain, compared to those who were aware.

Research by Sturzenegger et. al. (1995) states the followingset of variables predicted persistence of symptoms at 1 year:
“…unpreparedness at the time of impact….”
Primary research by Brault and Wheeler (1998) indicates that if the patient is caught by surprise during a rear-end collision, the threshold for injury begins at a change in velocity of only 2.5 mph.

                                            Head Position Factor
With respect to head position at the moment of impact, Turek states (1977):
“When the direction of force is from the side, or when a frontal or rear force occurs while the head is turned to one side, the spine is less flexible and the force is expended upon the articulations where the small bone elements may be fractured.”

Cailliet (1981) indicates that if the head is turned at the moment of impact, there is increased injury on the side to which the head is turned, as:
not only will the already narrowed foramen be compressed more, but the torque effect on the facets, capsules, and ligaments will be far more damaging.”

Web states (1985):
“When the hyperflexion-hyperextension or hyperextension-hyperflexion occurs with head rotation present, the pattern of tissue injury is different, and the extent of damage produced is always more severe.  Rotation increases stress in certain soft tissue structures, which then reach their limit of motion at an earlier point, thus resulting in more severe injury with less application of force.”
“It has also been shown that extension with pre-existing rotation is more likely to rupture the anterior longitudinal ligament than simple extension.”

Barnsley states (1993):
“If the head is in slight rotation, a rear – end impact will force the head into further rotation before extension occurs.  This has important consequences because cervical rotation prestresses various cervical structures, including the capsules of the zygapophseal joints, intervertebral discs, and the alar ligament complex, making them more susceptible to injury.”

Havsy states (1994):
Injuries are greater when nonsymmetrical loads are applied to the spine.  This occurs when the spine sustains a rotator injury.  The injuries are increased because the facet joints lock-out spinal motion, making the neck rigid, less resilient, and more susceptible to injury.
When the head is rotated 45° to one side, the amount of extension that side of the spine is capable of is decreased by 50%.  This results in increased compressive loads on the facet joints, articular pillars on the ipsilateral side, and increased tensor loads at the facet joints on the contra lateral side.  The intervertebral foramens are smaller on the side of rotation and lateral flexion, and the neurovascular bundles are more vulnerable to compressive injuries.”

Research by Sturzenegger et. al. (1994) state:
“Rotated and inclined head position both led to a significantly higher frequency of multiple symptoms and increased neck pain and headache intensity, and showed a trend to shorter latency of headache onset.   In addition, inclined head position caused more frequent cranial nerve or brain stream dysfunction and more frequent visual disturbances.  Both rotated and inclined head positions showed a significant relationship with signs of radicular deficit.”

Research by Sturzenegger et. al. (1995) states the following set of variables predicted persistence of symptoms at 1 year:
“…rotated or inclined head position…”
“Rotated as well as inclined head position showed a significantly higher incidence in the symptomatic group.”

Motor vehicle collision patient / passenger injury and clinical prognosis for recovery is not related to the damage of the vehicle.  Rather, the degree of injury and prognosis are coupled with acceleration of the struck vehicle, awareness of the patient, and head/neck rotation or inclination at the moment of impact.  In addition, there exists a myriad of variables, such as restraint placement, head restraint level, tissue elasticity, tissue strength, pre-accident joint degeneration, etc., that are impossible to accurately determine for any given collision.
                                                            Personal Injury Cases
  • Taking a good case history
  • Doing a thorough orthopedic and neurological examination from an expert chiropractor.
  • Taking good quality, adequate radiographs including stress views
  • Creating an accurate diagnosis that can be supported by history, complaints and examination findings
  • Doing standard and thorough daily charting
  • Duties under duress (DUD)
  • Loss of enjoyment of life (LOE)
  • Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
  • Doing periodic (monthly) thorough subjective and objective re-evaluations with follow-up written report of findings
  • Having referred if needed the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
  • Having referred to other health care providers and/or colleagues for verifying or additional opinions such as pain management specialist.
  • Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
  • Seeing a chiropractor such as Dr. Byers experienced in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation.                  
Ivancic PC, Pearson AM, Panjabi MM, Ito S. Injury of the anterior longitudinal ligament during whipash simulation. European Spine Journal 2004;13:61-68
Ono K, Kaneoka K, Wittek A, Kajzer J: Cervical injury mechanism based on the analysis of human cervical vertebral motion and head-neck-torso kinematics during low speed rear impacts. 41st Stapp Car 
Crash Conference Proceedings. SAE paper 973340, 339-356, 1997.
Siegmund GP, King DJ, Lawrence JM, Wheeler JB, Brault JR, Smith TA: Head/neck kinematic response of human subjects in low-speed rear-end collisions. SAE Technical Paper 973341, 357-385, 1997
Biomechanics Research Laboratory, Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, 333 Cedar Street, P.O. Box 208071, New Haven, CT 06520-8071, USA.
Panjabi MM, Ito S, Pearson AM, Ivancic PC. Injury mechanisms of the cervical intervertebral disc during simulated whiplash.  Spine (Phila Pa 1976). 2004 Jun 1;29(11):1217-25.
Ivancic PC, Pearson AM, Panjabi MM, Ito S. Injury of the anterior longitudinal ligament during whiplash simulation.  Eur Spine J. 2004 Feb;13(1):61-8. Epub 2003 Nov 14.

Ameis A, Cervical Whiplash:  Considerations in the Rehabilitation of Cervical Myofascial Injury, Canadian Family Physician, September, 1986.
Barnsley, in Spine:  State of the Art Reviews:  Cervical Flexion-Extension/Whiplash Injuries, Hanley & Belfus, Sept. 1993, p. 329
Batterman SD and Batterman SC; Delta-V, Spinal Trauma, and the Myth of the Minimal Damage Accident; Journal of Whiplash % Related Disorders; Vol. 1, No. 1, 2002
Brault JR and Wheeler JB, Clinical response of human subjects to rear-end automobile collisions; Archives of Physical Medicine and Rehabilitation; 1998, 79 (1): pp 72-80
Cailliet R, Neck and Arm Pain, F. A. Davis Company, 1981, p. 85
Cailliet R, Whiplash-Associated Diseases, AMA Press, 2006
Carroll C, McAfee P, Riley L, Objective findings for the diagnosis “whiplash”, J Musculoskeletal Medicine, March, 1986
Duffy, Michael F. MD; Stuberg, Wayne PhD; DeJong, Stacey MS; Gold, Kurt V. MD; Nystrom, N Ake MD, PhD; Case Report: Whiplash-Associated Disorder From Low-Velocity Bumper Car Collision: History, Evaluation, and Surgery; Spine:  Volume 29 (17) September 1, 2004 pp 1881 – 1884.
Emori RI, Horiguchi J, Whiplash in Low Speed Vehicle Collisions, SAE, Feb, 1990, p. 108.
Foreman S, Croft A, Whiplash Injuries, the Cervical Acceleration/Deceleration Syndrome, Williams & Wilkins, (1988).
Havsy, whiplash Injuries of the Cervical Spine and Their Clinical Seaquelae, Am Journal of Pain Management, January, 1994.
Henderson B; Putting the 5 mph injury threshold to the test; Personal Injury Law Journal; September 2006
Hirsh SA, Hirsch PJ, Hiramoto H, Weiss A, Whiplash Syndrome, Fact or Fiction, Orthopedic Clinics of North America, October 1988, p. 791.
Gun, Richard Townsend MB, BS; Osti, Orso Lorenzo MD, PhD; O’Riordan, Alison MPhil; Mpelasoka, Freddie PhD; Eckerwall, Claes Goran Mikael MD, PhD; Smyth, James Farrell; Risk Factors for Prolonged Disability After Whiplash Injury: A Prospective Study; Spine: Volume 30 (4), February 15, 2005, pp 386 – 391
Jackson, R, The Positive Findings in Neck Injuries; American Journal of Orthopedics, August-September, 1964, pp. 178 – 187.
Lord, in Spine:  State of the Art reviews:  cervical Flexion-Extension/Whiplash injuries, Hanley & Belfus, Sept. 1993, p. 360.
Macnab, in The Spine, Saunders, 1982, p.648.
McConnell WE, Howard RP, Van Poppel J, Krause R, Guzman HM, Bomar JB, Raddin JH, Benedict JV, Hatsell CP, Human head and neck kinematics after low velocity rear-end impacts – Understanding “Whiplash” SAE # 952724, 1995, 215-238
Nordhoff LS, Emori R, Collision dynamics  of vehicles and occupants, in Motor Vehicle Collision Injuries, Aspen, 1996, p. 288 and 290
Parmar HV, Raymakers R, Neck injuries from rear impact road traffic accidents: prognosis in persons seeking compensation, injury 24, (2), 1993, 75-78.
Pobereskin LH, Whiplash following rear end collisions: a prospective cohort study; journal of Neurology, Neurosurgery, and Psychiatry, August 2005; 76:1146-1151.
Robbins, MC, Lack of relationship between vehicle damage and occupant injury; Society of Automobile Engineers, February 1997, #970490, pp. 117-9.
Ryan GA, Taylor GW, Moore VM, Dolinis J, Neck strain in car occupants: injury:  injury status after 6 months crash-related factors, Injury, Sept. 1994, 533-537
Smith JJ, The Physics, Biomechanics and Statistics of Automobile Rear Impact Collisions, trial talk, June 1993, 10-14.
Sturzenegger M, DiStefano G, Radanov BP, Schnidrig A, Presenting symptoms and signs after whiplash injury:  The influence of accident mechanism, Neurology, 1995, 443-449.
Teasell, McCain, in painful Cervical Trauma, Williams and Wilkins, 1992, p, 293.
Teasell, in Spine: State of the Art reviews:  Cervical Flexion-Extension/Whiplash Injuries, hanley & Belfus, Sept. 1993, p.374
Turek, Orthopedics Principles and Their Applications, Lippincott, 1977, p.740.
Webb, Whiplash:  Mechanisms and Patterns of Tissue Injury, journal of the Australian Chiropractors’ Association, June, 1985.
Ommaya AK, Gennarelli TA: Cerebral concussion and traumatic unconsciousness.  Brain 97:6330654, 1974.
West DH, Gough JP, Harper TK: Low speed collision testing using human subjects. Accid Reconstr J 5(3):22-26, 1993.

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