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NEWS ITEMS - News-2014

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Does inflammation explains the complexity of whiplash associated disorders?

Because of a car accident, someone has a neck sprain. This results in tissue damage somewhere in the cervical spine, even though most often the exact tissue is not identified (through modern imaging methods). It might have been a small ligament, a joint capsule, or something else. Regardless of the type of tissue that is damaged, the sprain results in an inflammatory response. Contrary to what many people believe, inflammation is a good thing – it is our friend, at least in the early stage following injury. Inflammation cleans up the damaged tissue, so that new tissue can develop on a firm base. Hence, inflammation prepares the tissue for recovery and healing. However, the inflammatory phase should not last for more than a couple of days. If it lasts longer, it is often maladaptive.

A proper functioning of the body’s stress response systems, especially the HPA-axis (hypothalamus-pituitary-adrenal axis), is required for shutting down the inflammation in time. Cortisol is the major stress hormone produced by the HPA-axis, and it has strong capacity to shut down inflammation. Some patients with chronic pain following whiplash injury have a dysfunctional stress response system, making it plausible that chronic inflammation takes part of the pathophysiology of whiplash associated disorders. This important hypothesis was studied by Michele Sterling, James Elliott and Peter Cabot. They conducted a sound longitudinal study examining changes in blood markers of inflammation in the acute and chronic stage following whiplash trauma.

The inflammatory markers of interest here were C-reactive protein (CRP), interleukin 1ß (IL-1ß) and tumour necrosis factor a (TNF-a). When analysing the data of CRP, an acute phase protein which is regarded as a general (non-specific) marker of inflammation, a clear picture arises. In the acute stage, the entire whiplash group showed elevated CRP levels. However, at the chronic stage, only the whiplash patients with poor functional recovery had elevated CRP levels, while CRP levels had returned to the normal range in the recovered group. This indicates that ongoing inflammation explains (part of) the clinical picture in patients with chronic pain following whiplash injury, especially given the associations between CRP levels and sensory measures of central sensitization. Indeed, inflammation could serve as a source of ongoing nociception sustaining the processes involved in central sensitization, and inflammatory products like IL-1ß and TNF-a itself have the capacity to augment the sensitivity of the nervous system.

However, the findings regarding IL-1ß and TNF-a were not in line with this hypothesis. This does not imply that local tissue inflammation is not explanatory for chronic pain following whiplash. Circulating cytokines not always reflect tissue pathology, and the inflammatory response can be diverse and highly sophisticated, possibly explaining these conflicting findings.

At the very least, these compelling findings should trigger more studies examining the role of inflammation in chronic pain and disability following whiplash pain. The fact that the most non-specific marker of inflammation studied here (i.e. CRP) generated a picture of inflammation-mediated central sensitization in non-recovered whiplash patients, warrants more work in this area, which in the end could lead to improved health care for this underestimated medical problem.

Jo Nijs
2014 © Pain in Motion
Reference and further reading (full article available):
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0077903