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Putting An End to Chronic Pain After Whiplash Injury

Posted on: 12/11/2008
Scientists are still scratching their heads over chronic whiplash injuries. Why is it that some people recover just fine, while others go on to develop a chronic problem? In fact, the problem is common enough that it now has a label: whiplash associated disorder (WAD).

Some experts suggest there are risk factors that predict who might end up with WAD. One of those predictive factors is the focus of this study: local sensitization to noxious stimuli. This refers to how the nervous system seems overly sensitive and responds faster and with stronger pain signals in some people. The theory is that the nervous system is already pretty touchy either before the accident or right after the injury.

A prospective (observational) study was done to test this idea. A prospective study is a research effort that follows a group of people who are similar in some respects but different in other ways. In this study, two groups of WAD patients were tested and compared.

All participants in the study were seen within the first five days after they had a moderately severe whiplash injury. Everyone included was considered high-risk for WAD based on results of previous studies identifying risk factors. Risk factors for poor recovery include female gender, decreased active neck motion, and pain intensity after injury.

One group had recovered fully at the end of one year. The other group still had tenderness in the neck (and other regions) and was unable to return to a full work capacity. The groups were labeled recovered and nonrecovered.

This same group of researchers has done other studies in this area. They have shown that when the body perceives stimulation as painful, it produces muscle fatigue and weakness. The person who becomes highly sensitive has a lower threshold for pain. Not only that, but the pain spreads to other parts outside the area of injury. The affected muscles have a reduced ability to contract fully and also have reduced endurance (lasting power).

If patients who are at risk for WAD can be identified early enough, it may be possible to prevent persistent symptoms and preserve muscle function. The result could be a faster return to full function without loss of work capacity. It is not possible to test people for sensitization before an accident since we don't know when accidents are going to occur. The next best thing is to do what these scientists did: test patients right after the accident.

Muscle tenderness and mechano-sensitivity were measured 12 days after the whiplash injury and again after three months and at the end of one year. Nine areas of potential muscle tenderness were palpated. These tender points were located and tested bilaterally (on both sides). A score was given from zero (no pain) up to four (unbearable, untouchable) for each area.

A second test was done. This one measured stimulus-response between pressure and pain. In other words, pressure of varying amounts (from 50 kPa up to 800 kPa) was applied to three separate muscles in the body (trapezius/neck and shoulder, masseter/jaw, tibialis/lower leg). The pain response felt with any of the pressure gradients used was then scored from zero (no pain) to 10 (worst pain).

Almost one-quarter of the patients (22.9 per cent) had not recovered at the end of 12 months. Analyzing the data further, the authors made the following observations. There was no difference in type of work done (occupation) between the recovered and nonrecovered groups. Those who were in the nonrecovered group had more intense pain after the injury. They also had reduced neck motion after the injury compared to the recovered group.

Tenderness scores were higher for the nonrecovered group right from the start. Likewise, there was increased sensitivity to mechanical stimulation (pressure) and spread of symptoms in the nonrecovered group within days of the injury.

The results of this study show that there may be pre-injury factors that set a person up for the development of chronic pain after a whiplash injury. The exact mechanism for how and why this occurs remains unknown. Clearly, there is a decreased pain threshold and increased sensitivity to pressure or other stimulus that is then perceived as pain, but why does this happen?

Future studies will continue to look into this question. Scientists will try to understand exactly what's going on in the nervous system and why some patients seem more susceptible than others to WAD. Identifying predictive patient factors (personal or physiologic) can open the door to finding ways to keep pain signals from escalating in intensity, duration, and frequency. In this way, it may be possible to prevent WAD altogether.

Helge Kasch, et al. Deep Muscle Pain, Tender Points and Recovery in Acute Whiplash Patients: A 1-Year Follow-up Study. In Pain. November 15, 2008. Vol. 140. No. 1. Pp. 65-73.

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