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.


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


  1. I suffer from RSD have since May 1,2002. I go every 2weeks for SGB injections and trigger point injections. I have a morphine pain pump implanted but also take oain meds along with a lot of other meds. Yes I am still in pain 24/7. And my husband works 2nd shift and 6-7 days a week. He choose that shift so he could take me to my dr appt. but I spent 96% of my life home and alone. I have 1of my children that comes over now and then with 4 of my 10 grandchildren she helps me in anyway I need it. Sometimes I sit and wonder why I am here but then I see my husband come home. Or my daughter and grandchildren come over and I know. Just pain is something that is very difficult .

  2. Stephanie says:

    I am relieved to find good current information about CPRS.
    Am just now, one and a half years later, understanding the extent of this condition.

  3. GDay Howard –
    sorry this is so delayed – just to iterate from my email – great work and keep it up!
    best, L

  4. Hello Lorimer. I’ve been greatly impressed with your work for several years. I’m an internist at Providence Hospital and Wayne State University in Detroit and have conducted research in fibromyalgia (see Hsu, et. al., J Gen Int Med, 2010) using a model that links emotions to the onset and perpetuation of chronic pain. We are now in the second year of an RO1 ($3 million) from NIH/NIAMS to compare CBT versus an emotional expression program for fibromyalgia.

    I’d like to send you a complimentary copy of my book, Unlearn Your Pain, if you’re interested. Data from the 4-week program described in the book shows that 67% have at least a 30% reduction in chronic pain and 53% have at least a 50% reduction in chronic pain (mean duration of about 9 years) at a 6-month follow up point (soon to be published data).

    I’m currently revising my book and I’d like to include the story you tell in Painful Yarns about the snake bite. I frequently tell that story in lectures to illustrate important concepts about pain. By the way, I often add this at the end: “What is amazing is that the pain after a small scrape on Lorimer’s leg lasted for two weeks. He’s a pain researcher; he knows everything about pain; he knew that the pain up and down his leg was caused by nerve pathways; yet the pain persisted for two weeks! The nerve patterns were activated and took a while to calm down and reverse. But what might have happened if after one week, he went to his doctor and asked, ‘Why am I still having so much pain from a small scrape? And the doctor could say, “Oh, I’m afraid that you might have “post-snake bite venom” syndrome. It’s a chronic disorder, unknown cause, no effective treatment.” This is exactly the situation that occurs to people with fibromyalgia, whiplash, chronic fatigue and of course this leads to more fear, more resentment, more pain. Or what if during those two weeks, something was happening in Lorimer’s life: his son got arrested, his mother passed away, or his wife had an affair. That could trigger the same brain pathways that activate pain thus turning what would have been a self-limited disorder into a chronic one with little hope of cure.

    So, sorry for the long email. Would you mind if I used your story in my revised book, with credit to you, of course? Let me know if you’d like to see my book or communicate to further our attempts to really “explain pain.”

    Best, Howard

    Howard Schubiner, MD
    Director, Mind Body Medicine Center, Providence Hospital, Southfield, MI
    Clinical Professor, Wayne State University School of Medicine

  5. Paul Pratt says:

    Very interesting study for a person who has had RSD for 7 years.

  6. Phew. At least there is one other who gets excited by new CRPS papers. You know, slightly sweaty, mild increase in heart rate….

    I’m just going to use some imagery……yep, same response.