Stress, depression, blood flow and pain in CRPS – heading into the clinical data mine.

What do you get when a group of German neurologists publishes their clinical assessments from 118 patients with CRPS?  Excited, if you are me. OK, I am the first to admit that I am a bit odd in this regard, but I often feel so perplexed about the complexity of chronic pain that the opportunity to have a good look at this many data sets is one for which I am prepared to miss Cadel Evans crossing the line at the Arc de Triumph.  Fortunately, I only noticed this once the whole Tour de France thing was over, so I wasn’t really faced with that choice. I highly recommend having a look at this paper – it could be named after the first author – Voker Huge – but it is worth looking at the pictures at least – there are a few surprises. One of the surprises you cannot get from the pictures is the sheer scale of the assessment – my estimate is that it would have taken at least a couple of hours – probably more. There are so many measures that even with 118 participants, one runs a real risk of seeing something by chance – they see many things so the whispering in my mind is ‘which one is the false positive?’  Also, about 90 more patients contacted did not volunteer, so there is clearly a risk of selection bias here. Nonetheless, here are the things I thought particularly interesting:

  1. These CRPS patients had post-traumatic stress scores similar to those of people who have survived life-threatening events. They were, on the whole, depressed, and the stress and depression scores had a large relationship with spontaneous pain and disability, but not hyperalgesia. That is actually intriguing because it seems to argue against a real-time descending facilitatory effect, which I probably would have predicted.
  2. Degree of discolouration relates to spontaneous pain. This is interesting because it is a real time effect. Relevant to this is a recent study we are just about to submit that shows that we can modulate both temperature and pain according to where the affected arm is in space (oops! I can’t really tell you more just yet – I may get a wrap over the knuckles for even that!).
  3. Degree of sensory loss relates to pain and disability too. The sensory loss was large – an effect size of 1, even for the contralateral side of the body. That there is a widespread loss in mechanical and thermal detection strongly implies that the brain is behind it, at least to some extent. Importantly though, there is a bigger loss ipsilaterally which might imply small fibre neuropathy, the favoured explanation of some CRPS researchers (in fact, you should check out that argument if you are at all interested – it is a lovely paper even if it does not, in my view, address much of the dominant features of chronic CRPS).  The bilateral effect on sensory thresholds seems like the brain is inhibiting, or deploying less attention to, non-noxious input in general. That seems daft if one forgets that the brain is the villain behind the pain anyway, so perhaps any method to selectively increase modulators of pain might be in its interests, even if it is not in the interests of the human (aaagh I can feel the mind-brain-soul argument rearing its head).
  4. Pain and disability predicts motor abnormalities but not the other way around. This implies that the motor changes are really a result of things hurting. Of course, the only assessments were gross motor skills – there are no data for example on motor imagery stuff.

I thought the data were very consistent with a proposal we put out there a little while ago on the idea of a cortical body matrix that integrates autonomic control, spatial and somatotopic mapping, pain, protection, ownership and that disruption of this body matrix characterises much of what we see of efferent system disruption in chronic pain disorders. Then again, I have really just broken Darwin’s rule of spotting the things that DON’T fit with your paradigm, not the ones that do.  In closing – the paper for this is in PLOS, so you can lift the slides and everything – you just have to cite it.

About Lorimer Moseley

Lorimer is NHMRC Senior Research Fellow with twenty years clinical experience working with people in pain. After spending some time as a Nuffield Medical Research Fellow at Oxford University he returned to Australia in 2009 to take up an NHMRC Senior Research Fellowship at Neuroscience Research Australia (NeuRA). In 2011, he was appointed Professor of Clinical Neurosciences & the Inaugural Chair in Physiotherapy at the University of South Australia, Adelaide. He runs the Body in Mind research groups. He is the only Clinical Scientist to have knocked over a water tank tower in Outback Australia.

Link to Lorimer’s published research here. Downloadable PDFs here.

Reference

ResearchBlogging.org

Huge V, Lauchart M, Magerl W, Beyer A, Moehnle P, et al. 2011 Complex Interaction of Sensory and Motor Signs and Symptoms in Chronic CRPS. PLoS ONE 6(4): e18775.

Oaklander, A., & Fields, H. (2009). Is reflex sympathetic dystrophy/complex regional pain syndrome type I a small-fiber neuropathy? Annals of Neurology, 65 (6), 629-638 DOI: 10.1002/ana.21692