Can Injury Occur In Low Impact Motor Vehicle Collisions?

Today in 2008 its almost a foregone conclusion and certainly professional experience confirms that automobile accident insurance company claim adjusters, defense attorneys, and medical experts for the defense continue to proclaim that an individual within a vehicle involved in a collision cannot be injured if their vehicle sustains only minimum structural damage.

Yet there can be no doubt that individuals involved in minimum structural damage collisions not uncommonly develop symptomatology consistent with whiplash type neck distortion soft tissue injuries.

Health care providers both medical and chiropractic who examine these patients regularly document findings that are consistent with occult soft tissue trauma (alterations of segmental motion, alterations of joint end play, altered regional posture, alterations of normal tissue textures, abnormal sensitivity to local pressure, etc.).

With adamant and conformational claims by patients that their symptoms are genuine and substantiated by doctors that their findings are in fact real, ultimately has seemingly created the cynical perspective that the patient’s prime objective is secondary/monetary gain and the objective of the doctor is greed.

While the mathematical principles of ‘collision physics’ are complex and unique for each accident. They can in fact be simplified, as many of the forces involved are so small that for practical purposes they are negligible.

However, these principles often support the position of the patient and his/her doctor. The example used here is that of an automobile…

Rear Impact Collision In Which The Struck Vehicle Was Stationary At The Moment Of Collision…

The type of injuries chiropractors and medical physicians deal with frequently result from rear impact motor vehicle collisions that are classified as “inertial acceleration injuries.”

Popular terminology within both professions is “cervical acceleration / deceleration syndrome,” or CAD (Foreman and Croft).

The acceleration that results in passenger inertial injury is the result of energy. The acceleration achieved by the struck vehicle in a rear impact is dependent upon the weight and speed of the striking vehicle (Macnab).

Understanding energy is the key to understanding the physics of automobile rear impact collision vehicle damage and ultimately and most importantly for this articles purpose… passenger injury.

Published data on these principles of collision physics (Smith) indicate that the suppliers of energy are called sources, or Esources

In a rear impact collision the supplier of energy, or Esources is the kinetic energy of the striking vehicle.

The kinetic energy of the striking vehicle is dependent upon the striking vehicle’s weight and speed. This kinetic energy is mathematically represented as:

KEstriking vehicle = 1/2 m v2

Because of the sizeable mass that makes up a motor vehicle, even small speed collisions generate significant kinetic energy.

This kinetic energy is transferred into the struck vehicle. This kinetic energy is dissipated through several mechanisms, including the generation of sound, heat, vehicle crushing, and vehicle acceleration.

The energy dissipated through sound and heat are so small that they can be ignored as they are minor.

The energy that is dissipated through acceleration of the struck vehicle is critically important, as this is the energy that results in potential inertial acceleration injuries of the patients involved.

The energy that is dissipated through crushing of vehicles is important because this crushing is related to vehicle damage.

To make this complicated process completely clear:

The source of energy in a rear impact collision is the kinetic energy of the striking vehicle, or:
Esource = KEstriking vehicle

Published principles on collision physics (Smith) indicate that the receivers of energy are called sinks, or Esinks

In a rear impact collision there are two primary receivers of energy, or Esinks. They are the kinetic energies possessed by the two vehicles after the collision, and the energy that went into crushing or damaging the vehicles. The kinetic energies possessed by the two vehicles after the collision is represented by:

KEafter impact

The energy that went into crushing or damaging the vehicles after the collision is represented by:

VD, short for vehicle damage.

Restating the above: the receivers of energy in a rear impact collision is the kinetic energy of the vehicles after impact, plus the vehicle damage, or:

Esinks = KEafter impact + VD

The principle of conservation of energy requires that in an automobile collision the suppliers of energy must equal the receivers of energy. This energy balance equation is represented as:

Esource = Esinks

Since Esource = KEstriking vehicle and Esinks = KEafter impact + VD, we can write:

KEstriking vehicle = KEafter impact + VD

The most common injury from rear impacts are inertial acceleration injuries.

These inertial acceleration injuries are related to the kinetic energy after impact, or KEafter impact. By looking at this equation, it is obvious that the magnitude of passenger injury cannot be correlated to the amount of their vehicle damage.

In fact, the smaller the vehicle damage, the greater the kinetic energy available to cause injury. This effect is especially relevant in low speed rear impacts (Navin and Romilly, Smith, Nordhoff and Emori, Robbins).

The development of safety or “no-damage” bumpers has been the standard for several decades. They are designed specifically to minimize vehicle damage in low speed rear impact collisions, and there is clear evidence that insurance property losses have decreased dramatically as a result (Smith).

Studies clearly indicate that such 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 the kinetic energy that causes patient injury.

Current bumper standards have the effect of reducing property damage while subjecting the occupants to a more violent ride and increasing 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 of 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.”

Macnab 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 struck 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 imparted, the moment of inertia of the struck vehicle, and the amount of collapse of force dissemination by the crumpling of the vehicle.

Ameis 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 or 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.”

Importantly, published studies have reviewed both the presenting and long-term clinical status of consecutive patients injured 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 bore 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 conclude:

“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) followed 117 consecutive whiplash patients 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 that proclaims one cannot sustain whiplash injury in low speed accidents is scientifically and methodologically flawed and invalid.

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:

“The myriad of dynamic variables between occupant and vehicle precludes a definition of change-in-velocity thresholds for neck injury from car collisions.”

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 the kinetic energy that creates occupant injury is increased, as explained above.

A second part of the answer is that these low speed rear impacts are capable of producing high accelerations to the vehicle occupants. McConnell et. al. (1995) analyzed the head and neck kinematics of eighteen human volunteers subjected to rear impacts between 3.6 – 6.8 mph. All volunteers were male of apparently good health, and of course 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 G’s during the period up to 150 msec after the impact.

The third 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.

Awareness Factor

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 possess 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 motion segment 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 Sturzenegger et. al. (1994) state:

“Patients struck when they were unprepared for the impact had a significantly higher frequency of multiple symptoms, higher headache intensity, and shorter latency of headache onset.

The state of preparedness proved to be the first significant factor with respect to initial injury findings.”

Research by Ryan et. al. (1994) state:

“…awareness appears to have a strong protective 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 persisting symptoms and/or signs of neck strain, compared to those who were aware.

Subjects who were unaware of the impending collision were 15 times more likely to have a persisting condition than those who were aware.”

Research by Sturzenegger et. al. (1995) states the following set 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.”

Webb 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 rotatory 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 contralateral side. The intervertebral foramen 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 brainstem 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) state 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.”

Conclusion

Motor vehicle collision patient/passenger injury and clinical prognosis for recovery is not related to the damage of their vehicle. Rather, degree of injury and prognosis are coupled with direction of impact (rear-end), awareness, and head/neck rotation or inclination.

References

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