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Whiplash or cervical acceleration/deceleration syndrome

Around half of the patients with neck pain after whiplash will develop chronic pain. Changes in brain structure which are related to with pain, disability and other neurological changes, as well as the brain function, have been found in people with chronic whiplash. Research has found structural and functional brain differences between people who develop chronic low back pain compared to those who recover but research like this is still lacking in people with whiplash.

So what is whiplash? For a start a more appropriate term might be cervical acceleration/deceleration syndrome. The word syndrome indicates that it is not just one simple thing. Whiplash was first describe in 1928 and since then it has been a Pandora’s box for researchers, given its strong association with litigation. But the chief complaints are pretty consistent amongst sufferers.The most common is neck pain, but there can also be headache, blurred vision, tinnitus, dizziness, nausea, paraesthesias, numbness and back pain. Yet all of these have defied casual clinical explanation. The trouble is that those who suffer are also thought to be fabricating pain in order to get a payout, or even hypochondriacs using the injury for some other type of gain.

However time has demonstrated that litigation is neither the cause, nor the cure for this type of injury. In fact research has indicated that 2 years after payout, 45 % of people were still suffering, and that is only those who responded to the researchers questions.

Some researchers have shown that whiplash, in the absence of blunt head trauma, may result in small bleeds on the surface of the brain and concussion and bruising under the sheath covering the brain. We know that concussion can lead to headaches or post traumatic headache syndrome but this is usually after direct head trauma. However car accidents are a cause of fatal and not fatal brain injuries, the latter occurring without a direct trauma to the head.

The term whiplash is worth looking at here and as the title above indicates a different term might be more appropriate. There are, in the process of the accident both flexion (forward) and extension (backward) movements. The high force at which these movements occur alongside a rotation of the head and neck create significant soft and hard tissue injury within what would be considered normal range of movement, thus making this injury unique. The term whiplash has been associated with head and neck injury coming from all directors but the rear impact injury is the more significant, But the term is too vague to be suitable for clinical use and thus acceleration/deceleration is more appropriate.

The mechanism of injury is worth noting as it is not a simple forward and backward movement of the head and neck.

The first thing to consider is the size of the vehicles. If a larger car hits a smaller car both the car and the occupant with incur less damage. If the opposite is the case the occupants of the larger car will also receive less significant injury. There is also an argument that seat belts can actually increase the damaging forces to the head and neck at low speed and some research has indicated that seat belts, safety bumpers and head restraints actually lead to more significant occupant energy impulses.

The sequence of events are more complex that one might initially think and yet their very explanation indicates why this is such a significant injury.

Phase one, after a rear impact accident both cars quickly reach a common speed. The one in front accelerating and one behind decelerating, typically. For the occupant of the front car, the torso is forced back into the seat, the head and neck are initially fixed and the vehicle moves forwards underneath them, causing the neck, upper and lower back to straighten. This causes the neck to be compressed. At the end of this rearward translation the head and neck begin to extend backwards and the neck is exposed to very high tensile forces stretching the neck upwards.

It is during the next phase that the joints of the jaw can be injured. The link between this type of accident and jaw dysfunction is well documented. IThe theory is the jaw is forced forwards causing damage to connective tissue and to structures in the joint itself. The mechanism is that the jaw is opened ‘in reverse’ as the head is thrown back into extension in the first milliseconds after impact. Because there is no voluntary muscular contraction there is no control and the opening of the jaw beyond 25 degrees leads to severe sprain of the joint capsule and compression of the disc that sits between the two bone surfaces.

In this second phase the seat back, which has been loaded with elastic energy, will begin to return to its original position and this coincides with a change of direction of the torso. This return of the seat back may mean that the torso is accelerating faster than the car. After impact the torso will rise up and move backwards creating some slack in the seat belt across the lap and shoulder. Also, even if the brake pedal has been pressed, this rearward movement will pull the foot off the brake, increasing the acceleration. At this point with the car and torso at maximum acceleration, the head is only just beginning to accelerate.

Phase 3: during this phase the head and torso are at peak acceleration while the vehicle is beginning to slow. Any slack in the seatbelt allows the pelvis head and torso to move forwards increasing the potential for injury in the final phase. At this stage the brake pedal may be reengaged increasing the speed of deceleration leading to greater rotational forces in the neck and cervical spine.

Phase 4: In this the final phase the car is no longer accelerating, the head and neck are in full deceleration. The seatbelt will abruptly halt the torso but the head will continue to slow down unrestrained in a forward arc. Acute and violent bending will occur at the lower cervical and cervicothroacic spine and it is this that is probably most responsible for the majority of ligamentous and muscular soft tissue injury.

Given all the above the main issue remains the question of the forces generated. Litigation would contend that, at 8mph and with minimal damage to a car, the claim for injury is fabricated. But when talking about forces, and we are talking about the conventional G forces as per the earth’s gravitational force. This is 9.81m/sec. The forces developed at the head are 2-2.5 times that of the struck vehicle and could be up to 5x the input acceleration. So for an input that produces an acceleration of 12G the resulting horizontal acceleration is greater than 50G for about 40milliseconds. That kind of force going through soft tissues is enough to cause significant if microscopic injury.

Continuing on the theme of the potential for damage, most of the early motion in the neck as the torso accelerates underneath produces a shearing of the neck followed by the beginnings of rotation at the top of the spine. It is at this point that shearing and bending are at their maximum.

The initial position of the neck at impact is significant. With a slight forward bend the sequence after acceleration is:

a) compression of the entire cervical spine

b) marked flexion in the second phase

c) rotation of the head in the forward direction (a concertina effect) followed by hyperextension

There is disagreement about which phase and which position causes the most damage but it is known that the deceleration forces of the flexion phase are greater than the acceleration forces in the extension phase.

Besides causing soft tissue and hard tissue damage to the neck, there is also a high likelihood of concussion. If a rear collision accelerates a car to 10.8mph in 100milliseconds there is a 50% chance of sustaining a cerebral concussion. Side impacts and whiplash motions are more likely to result in diffuse type of injury that most responsible for brain injury.

Sitting posture has a significant influence on the likelihood of injury. The effectiveness of head restraints in reducing whiplash injury is inversely proportional to the distance between the occupants head and the restraint. So if you slouch you have a head forward posture. Therefore the ability of the head restraint to protect against neck injury drops off sharply. The rebound of the head off the head restraint leads to an increased acceleration. Similarly if the restraint is too low then the head will extend above and over the restraint that will then act as a fulcrum, intensifying the problem with upper cervical extension/traction injury.

Even if the restraint is in the ideal position and the head is within 2 inches there are two possible issues:

  1. with the elastic recoil of the head restraint, the head will be catapulted forward leading to rebound injury and

  2. immediately after head impact at the base of the skull the upper neck will be forced into flexion leading to a compression injury.

All the above goes to show that whiplash is not a simple injury. The forces on and the movements of the body combine to make even the most innocuous shunt a significant event, one that should be taken seriously not only by the victim but also by the medical and legal professions.

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