Well, we didn’t actually have coffee. But I think I may have been drinking coffee and done a spit-take when I opened my inbox to find that Lorimer Moseley had responded to an insanely long, and question laden email I sent him about a year and a half ago. Tweets had stirred up confusion in my mind over our new understanding of pain developed through the work of he and David Butler. Together, they have guided us into a new world where pain is now understood as a product or output of the brain. The brain is the decision maker as to whether or not a particular signal or input is dangerous enough to warrant a pain response or output. The brain evaluates and estimates the threat based on multiple areas of input: history, emotion, experience, etc., not simply how hard did you fall or how hard were you hit.

 Moseley has pioneered the use of motor imagery to address chronic pain states. Providing new inputs through imagery to influence the brains output. In his book, Painful Yarns, he highlighted the story of a man injured in a bread factory accident that had a severe increase in his CRPS (Chronic Regional Pain Syndrome) every Saturday morning. They finally figured out the trigger for his routine Saturday symptom increase was the scent of his neighbor baking bread. Scent input triggered a perceived threat by his brain, which then ramped up and produced the pain output. Chronic pain, not to oversimplify, is an overprotective brain, misinterpreting input and using pain signals as a warning.

 I attended a conference in which Lorimer and Paul Hodges team taught these concepts and others regarding the changes in the brain that occur with muscular training. I left with a loose grasp on the concepts, but was still working out the application of it clinically in my primarily non-chronic pain patient population, when the tweets began….

 So I wrote Lorimer a note. Excerpts are below:

 (JW) At the Fall conference, you talked about output, and Hodges about the influence and changes we see in the brain due to input, it seemed a perfect pairing of information. Input and output intermingled. Creating clinical models around that intermingling in multiple populations is the key and at the heart of why I am writing. So if you have a moment…I have some questions to help me communicate to my patients, and myself how this all gets translated into practice. The messaging in social media and blogs out there is getting a bit confusing, and lack practical steps for application. 

 People are tweeting stuff like this: 

” Pain has never been shown to be caused by the length and strength of muscles. Lets stop telling patients otherwise. #solvePT #PainPT“

 So if we follow the logic of this statement, then why do we bother to strengthen? Is that what we should be telling people instead, don’t bother, b/c the evidence shows strength has nothing to do with resolution of your pain? That doesn’t fit with my interpretation of the blend of your work with Hodges work. But perhaps I am missing something, which is why I am writing. In terms of the all important emotional piece, is the capacity to take action in your pain through say exercise an empowering positive emotional input?

(LM) I would say it is, but that does not stand in contradiction to the statement from twitter above. 

If for example, the injured tissue involved is say a nail hammered into the back of a patients hand, and the patient hits the hammer over and over again throughout the day….shouldn’t we do something about that, get the patient to stop that? And of course call for a psyche consult. A tongue and cheek way of asking do we run the risk of throwing the baby out with the bath water by not appreciating neuromuscular and mechanical inputs, too (repeated through movement patterning or faulty alignments or bad habits)? 

Well, of course we should do something about that. I think you are not thinking of an actual patient here, BUT, you might be thinking of a patient you consider to be continually provoking a nociceptor in the tissues. Then of course you should fix this. The tricky thing is that it can be difficult to demonstrate the nail in the hand effect and many of our tests are not quite as specific as we thought. Still, your argument stands I reckon.

  Poor motor control, alignment, shearing forces, weakness, etc all of our previous theories about why we experience pain, do they still hold some merit if essentially they are metaphorically hammering the nail in a little bit deeper each day? If graded motor imagery is a way to change input to the somatosensory cortex to create a change in the brains output, can form, movement, alignment, muscle recruitment strategies, ANS involvement, etc also be inputs to change the brain’s outputs? If not, then why do peripheral treatments seem to improve pain (or reduce the brains interpretation of threat)? Hodges work leads me to believe we can actually change the brain with some of our training ideas.

I think there is very, very good evidence that we can change the brain by training. Paul’s work adds to a very large body of evidence in this regard. But what has really changed is Paul’s interpretation of that work, which I think is a sensible change, is that the training might be having its main effect in the brain, rather than in the forward shift, by 20ms, of contraction of a particular – not very high impact biomechanically – muscle. The thing that is difficult is interpreting it all – motor control training is not simply that – it is also a conceptual package, graded exposure, cognitive therapy, behavioural therapy. That M1 (Primary Motor Cortex) changes is lovely and interesting, why it changes is PROBABLY due to the contraction, why it changes functionally is very difficult to know, and whether it relates to pain relief is impossible at the moment to work out.

 Is there a distinction between how the brain produces “regular” old pain (like a nail driven into your hand) vs phantom pain in that same hand after the nail hammering behavior has stopped? Should their clinical programs be different? 

Yes. In the former the clinician should reason honestly and in an informed way and end up removing the nail, but the latter, the clinicians should also reason, there is no nail to remove so the treatment should be different. Both treatments might contain common elements of course. 

 Isn’t there a way of communicating this so that both inputs and outputs are considered and have some value (input and output intermingled)? Is it just how we are communicating causality? Or am I just lost?? 

 You are clearly searching and I LOVE this. I hear myself in some of this. The questions that I found most difficult to answer without learning more, and then more etc., etc. (the old the more I know the more I realise I don’t know etc. thing) – are questions like ‘did I ONLY change form? Recruitment? Alignment? Etc? or did I inadvertently do many things.

Again, my questions in part are born out of a lot of the social media trickle down from your work, particularly a lot of statements that I think communicate throwing the baby out with the bath water as we try to create clinical programs. I am not trying to create the message, but came to the source to clarify for those of us in the trenches trying to integrate the info in multiple patient populations. I think (hope?) I am not alone trying to decipher it. 

 I don’t reckon you would be. I am also trying to work it out. A common misinterpretation of my work is that I think that there is no point thinking about primary nociceptive input in people with pain. I do not think this and I do not think I would ever have said this. What I do think is that there is compelling evidence that the relationship between pain and tissue damage is seldom simple and is sometimes very tenuous indeed. 

 Thank you for your time, I really appreciate it. 

and I yours.

L

Awesome…right?

 I was so grateful for all of Lorimer’s insight, and his continued kindness in HOW he delivers his message. Please take note bloggers, and social media users, think WWLD before you tweet or blog. I had some great takeaway’s that have guided my own practice and teaching since this conversation a year and a half ago. First, I really liked that we can earnestly say, that we aren’t really sure why a lot of what we do works, but we are trying to figure it out! And just because we don’t understand the why, it doesn’t negate that our interventions can bring change and help. I can live in that uncomfortable unknown…how about you?

 Also, when we change a piece of the puzzle through a peripheral intervention, we likely change multiple inputs at once. It is hard to point to the one thing that ultimately caused the change in pain…that is what our old idea of pain as input promoted and what we can no longer support in the new pain paradigm.

 Lorimer’s final point has provided the greatest clarification for me as I slog through the social media pontification and pundits. More importantly as I apply these ideas clinically. “A common misinterpretation of my work is that I think that there is no point thinking about primary nociceptive input in people with pain. I do not think this and I do not think I would ever have said this.”  

 And how comforting is it that he is “still trying to work it out”, too.

 Thanks again to Lorimer. He is a great communicator and teacher, moving us all forward!

 To learn more about the new pain science paradigm, check out:  Explain Pain and Painful Yarns.