I'm on a bit of a stress-response system 'kick' these days. The more findings about whiplash emerge, the more I feel like what we're dealing with in the case of neck pain of traumatic origin (ie. whiplash or whiplash-associated disorder) is less about the tissue damage that has occured, and more about the response of the organism to the whole experience.
Consider the fact that, on balance, there is relatively little evidence in support of a single tissue lesion that can account for the myriad possible signs and symptoms of WAD. What we tend to get are research groups finding that, usually in some subgroup of patients, there is an association between WAD symptoms and a particular tissue lesion, such as Bogduk's zygapophyseal joint findings in the mid-90's, or Kaale's alar ligament findings in the mid-2000's as examples. Pretty much any tissue you can think of in the neck, or beyond, has been implicated at some point as the driver of WAD symptoms. But generally these findings have either not been replicated, or don't stand up, when independent research groups attempt the same thing. These kinds of findings led the Neck Pain Task Force to conclude that there were no really good diagnostic tests available in 2008 for identifying non-catastrophic lesions in the neck.
But as we all know from the world of pain, the absence of visible pathology does not mean that a condition doesn't exist. WAD is clearly a real, and at times quite debilitating, condition. There have been several proposed mechanisms for why some people recover uneventfully while others toil with persistent problems. The specific tissue lesion models represent one such proposed pathway. Others include the cognitive-behavioural or 'fear-avoidance' pathway(s), the 'medicolegal context' models, expectation, coping strategies, etc, etc... Lots of suggestions, little clear direction.
When I consider any or all of these pathways, I come back to the idea of stress, or distress (a term I'll use from here on forward to discriminate negative stress from positive stress), as a coalescing model for all of them. Consider the work coming out of CONROD at the University of Queensland. Dr. Michele Sterling and her colleagues have shown us that post-traumatic stress symptoms seem to be a risk factor for persistent problems. When Dr. Jim Elliot was there, he began his work evaluating fatty infiltration in the deep muscles of the neck (extensors and flexors), and found that people with chronic WAD had statistically and clinically greater ratios of fat:muscle. The strongest predictor of deep neck muscle fatty infiltration was...post-traumatic stress symptoms in the acute phase of injury.
Fear, catastrophizing, post-traumatic stress, depression - they could all be largely classified into that amorphous construct of 'distress'. And of course, stress doesn't have to be emotional, it can be physical as well. Extreme heat is a stressor, as is extreme cold, as two clear examples. Both represent potential threats to not only homeostasis but our physical well-being, and both will stimulate some kind of coping strategy in order to attempt to maintain homeostasis. Surely pain and injury could also be regarded as stressors. Add pain and injury to a highly traumatizing experience, such as a car accident, that occurs within a highly medicalized and litigious environment, and we've got the perfect recipe for an exaggerated or dysfunctional stress response.
When I think stress-response, I think of the hypothalamic-pituitary-adrenal axis, part of the sympathetic-adrenal-medullary axis. Activity in the axis, stimulated by either emotional or physical stress, culminates in the release of the stress hormone cortisol. Cortisol serves plenty of good functions, mostly in priming our bodies for fight, flight or freeze. In the short term, it's a life-saver. But get too much of it, or get a little of it over a long period, and things start to turn sour. Chronic inflammation (through its influence on cytokine activity), sleep disturbance, muscle atrophy (breaking down protein for energy), cognitive disturbances, general body pain - wait a minute, this is starting to sound a lot like some other conditions I can think of. Indeed, a colleague of mine Dr. Stan Van Uum has recently shown that cortisol levels in the hair of people with severe chronic pain is considerably higher than of that in age- and sex-matched controls, which is a good indication of long-term stress. And Dr. Janice Kiecolt-Glaser, a pioneer in the field of psychoneuroimmunology, has done considerable work in this area - the most relevant being a demonstration of how stress slows wound healing.
What I like about this conceptualization is that it brings the mind and body together. I've always had a problem with purely cognitive (fear) models, or purely biological, or purely social models. They've always seemed to focused on a single mechanism. Surely someone doesn't develop chronic pain simply by virtue of being afraid of pain. There was always a connection missing for me, and I think I've found it in this whole stress-response field.
We're currently running a study to evaluate exactly this hypothesis. Any of you in the London area who see people with acute whiplash are encouraged to direct your patients to our home page for a description of the study and how to get involved. As always, feel free to leave comments on this post in the space below.