Motor Vehicle Accidents
Vehicle Damage is not equal to Occupant Injury and Disability.
Considerable attention in medical literature has been given to the relationship that exists between bodily injury relative to the damage sustained by the motor vehicle involved in the accident. To take an extreme example, if a motor vehicle had its tires set into cement, then was rear ended, it is possible that the damage to the vehicle could be extensive, and the bodily trauma virtually non-existent because the vehicle could not more forward (acceleration). Utilizing this same example, in a typical rear-end collision, the acceleration involved is usually the primary case of soft tissue injury. This is simply an example of Newton's First Law, the Law of Inertia. The fact that a motor vehicle is not totally stationary (as most vehicles are not imbedded in concrete), is more likely to cause less damage to the vehicle and greater injury to the occupant.
There are many individuals (and insurance company claim adjusters) that have the belief that vehicles equipped with air bags and restraints provide adequate protection of the inhabitants of the vehicle, and are capable of preventing any injury. This is a false belief. Motor vehicles are equipped with safety restraints based on an average male. Unless you know, and can correct head restraint positioning, the restraint can actually be responsible for worse injury during impact. The sudden and usually unexpected deployment of air bags can produce rapid restraint of a body moving forward, jerking the body to a spot and/or in some cases causing a sudden reversal and pushing the body backwards. Shoulder and lap belts can do an admirable job of restraining the torso and pelvis. However they do little in preventing the whiplash action that can cause serious injury to the neck and head. And, as previously stated, only if the shoulder and lap restraints are correctly positioned.
There are numerous references in the available literature that document that symptoms of a whiplash injury can appear immediately following the injury, hours later, days later, or even weeks later. In addition, the persistent and disabling symptomatology in most whiplash cases is due to the damage and involvement of the delicate and vital nerves and blood vessels in the spine (soft tissue injury). The healing time of these soft tissue structures may be prolonged for months or even years after the injury.
There is also great concern involving the complaint of low back pain following an acceleration and deceleration (whiplash) type injury. The scenario involved goes something like this:
A person is involved in a rear end collision. The individual is utilizing restraints and the vehicle is equipped with head restraints. In the time immediately following the collision, the individual experiences neck pain and headaches. The person seeks care for those symptoms. Some time after, the person begins to experience lower back pain. However, the individual may seek to find a different cause of the lower back pain, or the person may be convinced by a claim adjuster or another that the lower back pain must be caused by a source other than the collision.
However, studies have shown us that there is a clinical relationship between acceleration and deceleration injuries with subsequent low back complications. The low back onset may be delayed for months after that accident. This is primarily due to the biomechanical relationship between the cervical spine (neck) and lumbar spine (low back). In one study, it was shown that 85% of patients that sustained neck injuries as a result of whiplash, developed low back pain some time after the motor vehicle accident. Of that 85%, over half developed the low back pain 4-6 months after the injury and almost all of the rest 7-12 months after the initial accident.
Rear end collisions are not the only cause of whiplash type injury. In a rear end collision, the mechanism of this injury is forceful hyperextension and secondary hypereflexion. In a side collision, the mechanism of injury is forceful lateral flexion to the side of impact, then secondary lateral flexion to the fopperies site of impact. In a head-on collision, the mechanism of injury is forceful hyperflexion and secondary hyperextension.