Chronic Pain II: A Different Perspective

Dr. Edmund Bruce-Gardner

So after reading the last few blogs, hopefully you have a bit more understanding about how pain works, and why sometimes we hurt when there doesn’t seem to be any obvious cause.

The question then becomes “OK, I understand that pain is an output, and is influenced by all these different factors separate to the signals coming form the body.  But what can I do about my chronic pain??”

The first answer seems maddeningly unhelpful. Just because you intellectually “understand” something, does not mean that you understand it, in the sense of knowing it and believing it ‘in your bones’.  

​So the first thing you have to do, is go back and re-read all the stuff you just finished about pain being an output, multi-factorial, and not related to damage. 

​Think about it: if someone describes to you how you play a tennis shot, for example, you might well understand what they are describing, but I very much doubt you will be on Centre Court at Wimbledon next year!

Sometimes a different way of explaining things can click where previous elucidations were, well, as clear as mud! So try to read as many different accounts of pain and how it works as you can.

One common metaphor that seems to be helpful for a lot of people is the idea of a fuse.

When something happens in the body, like twisting your ankle, information about the potential damage (stretch or compression in the tissues etc) travels up the nerve.
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We can visualise this like a fuse burning in a cartoon. 

​When it gets to the spinal cord, it has to ‘jump’ a little gap, called a synapse, before continuing up the spinal cord to the brain. Various factors can affect the strength of these signals. 

​Some, like endorphins (chemicals that reduce pain and stress), adrenaline (I think everyone’s heard of that one!) and cortisol (the ‘stress hormone’, which can intensify the pain experience[1],[2],[3]), are neurotransmitters or hormones, chemicals that interact with receptors in different area of the body to change the way things work.

Others are interactions between various parts of the brain with very long, complicated names like rostroventromedial medulla or anterior cingulate cortex, leading to a complex relationship between areas involved with emotion, cognition, motivation and sensation.

​It’s all very complicated, and the thing to remember is that these other influences can both facilitate (increase) or inhibit (decrease) the strength of the signal that we identify as pain. 

​The second really important point is that these factors are much, much stronger than the original signal itself, like a couple of hundred times stronger!

​Going back to our fuse metaphor, we can think of the inhibitory factors as buckets of water.
Imagine what happens when we throw two hundred-odd buckets of water on some little fuse… That’s right! It goes out. We don’t feel any pain. 
​This is often what happens when we get injured while playing sports: because there is a big surge of adrenaline, it hurts a lot less than it does, say, five or six hours later.

The facilitatory factors we can think of as buckets of petrol. Again, it doesn’t require Sherlock Holmes-like analytical skills to deduce that these might intensify that fuse burning, leading to a greater perception of pain. 

Note: these ideas of ‘petrol’ and ‘water’ are functionally identical to the notions of DIMS and SIMS used the NOI group, as described in the previous chronic pain blogs.

So whatever the signals are coming up from the body, whether or not we see them as pain depends on a whole host of other factors. Remember our axiom from the previous blogs:
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Pain is the label your body attaches to something when it feels it has more [credible] evidence of threat, than of safety.

​The more we learn about how pain works, the smaller part those original signals seem to play when it comes to the brain ‘deciding’ what is credible evidence.
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If you have more buckets of water than petrol, no pain; and vice versa.

​As mentioned, the processes involved in chronic pain are different to acute. In fact, neuroimaging studies have shown that chronic pain may be accompanied by changes to structural features, functional connectivity and activity of key brain regions[4],[5],[6].

So, whatever else, you don’t need to worry that the pain is just in your head.
​Well, except that your brain is inside your head (it would be worrying were it not).  Dammit, you know what I mean.

​So there are physical things going on, but these are influenced and modulated by well, pretty much everything else. 

Many of the brain sites identified as being involved with the processing of noxious stimuli are generally involved with emotional systems. It’s been said before, but it bears repeating: How you think and feel about your pain changes the way you feel your pain. 

​It stands to reason, then, that if we change the ways we think and feel about our pain, the way we feel the pain will also change!

​So it might seem frustrating, because you already feel you’ve done all of this to death, what with the specialist, your osteo, the occupational therapist, and pain management clinic (if you’ve gotten that far) all banging on about the need for education and understanding.

On a side note, if all of these disparate professionals all agree on something, that’s worth sitting up and taking note in and of itself!  Consensus in science is a good thing, it doesn’t indicate conspiracy

But speaking purely personally, as my understanding of pain, and my issues, has developed and deepened over the years, there is less and less… …emotional content, I suppose, attached to it. I tend to perceive it much more as my body trying to tell me something (whether or not its concern is justified is a different story!), rather than that gut-wrenching sensation of wrongness.

So again, as redundant as it seems, step one really is going back and reading, and re-reading, everything you can find (and understand! The research itself can be pretty heavy going!) on pain and the brain.

Ask your osteopath for some resources if you feel like you need a some inspiration and a fresh approach!

The next blog will deal with Step Two, where we start putting some of this theory into practice.

References

​[1] The biochemical and neuroendocrine bases of the hyperalgesic nocebo effect.
Benedetti F, Amanzio M, Vighetti S, Asteggiano G
J Neurosci. 2006 Nov 15; 26(46):12014-22.

[2] Nocebo hyperalgesia: how anxiety is turned into pain.
Colloca L, Benedetti F
Curr Opin Anaesthesiol. 2007 Oct; 20(5):435-9.

[3] Isolating the modulatory effect of expectation on pain transmission: a functional magnetic resonance imaging study.
Keltner JR, Furst A, Fan C, Redfern R, Inglis B, Fields HL
J Neurosci. 2006 Apr 19; 26(16):4437-43.

​[4] Wood P, Schweinhardt P, Jaeger E, et al. Fibromyalgia patients show an abnormal dopamine response to pain. Eur J Neurosci. 2007;25:3576–3582

[5] Baliki MN, Geha PY, Fields HL, Apkarian AV. Predicting value of pain and analgesia: nucleus accumbens response to noxious stimuli changes in the presence of chronic pain. Neuron. 2010;66:149–160.

[6] Baliki M, Petre B, Torbey S, et al. Corticostriatal functional connectivity predicts transition to chronic back pain. Nat Neurosci. 2012;15:1117–1119.