Pain may or may not inhibit (chronic low back) pain

In 2014 David Yarnitsky hypothesised that people may be characterised by profiles that vary from pro- to anti-nociceptive. Those with pro-nociceptive profiles would likely show a reduced capacity to enrol the body’s own pain inhibitory mechanisms, and heightened sensitivity to repetitive, painful stimuli. Those with anti-nociceptive profiles would demonstrate the opposite.

Testing conditioned pain modulation (CPM) exploits the old idea that “pain inhibits pain”. A painful “test stimulus” is applied in the presence, and absence, of a painful “conditioning stimulus”. If the test stimulus is perceived to be less painful when the conditioning stimulus is applied, pain is thought to have inhibited pain by getting the body’s own pain inhibitory mechanisms working.

When I was an undergraduate student I remember one of my lecturers describing the use of ultraviolet lamps to burn the skin on the shoulders of people with low back pain so that they had a more painful problem elsewhere in their body, in the belief that they would then feel less back pain. Now, that was over 20 years ago, but until recently little research had been done on pain inhibiting pain in people with back pain.

Together with colleagues at Curtin University, we have just published paper in the journal Manual Therapy, exploring CPM in people with chronic low back pain (CLBP) [1]. We applied pressure to the low back that led to the perception of pain, then heated up their hand, again to the point of pain (but not to the point of frying their skin!), then re-tested how much pain they perceived when we applied the same amount of pressure as before. We also did this in people who had never had any longstanding pain (71 people per group). The results were significantly different between the groups.

Seventy-three percent of people with CLBP had a facilitatory response: they perceived the pressure stimulus as more painful when their hand was heated up than when it wasn’t. This suggests that in the majority of people with CLBP their body’s own pain inhibitory mechanisms are not working very well at all. Pain did not inhibit pain, it just ramped it up even more. However, a facilitatory response was also found in 31% of the healthy participants. In some people pain did actually inhibit pain (11% of people with CLBP, compared to 36% of people with no pain). In the remainder the application of the conditioning stimulus made no real difference.

So this study may fit with Yarnitsky’s hypothesis, which goes on to suggest that a pro-nociceptive profile may be associated with chronic pain. This may also mean that those healthy participants showing a facilitatory CPM response may be pre-disposed to the development of a painful disorder, but this is currently unknown. More importantly, our results suggest that we should not go around burning the shoulders of people with CLBP with ultraviolet lamps, as it will just make them worse.

P.s. I haven’t been near an ultraviolet lamp since those undergraduate days. I wonder why?

About Martin Rabey

Martin RabeyMartin is a Specialist Musculoskeletal Physiotherapist (as awarded by the Australian College of Physiotherapists), and has just submitted his PhD at Curtin University in Perth, examining the complex interactions between factors which make low back pain persist. He moved to Sydney a year ago, and continues to research low back pain at Neuroscience Research Australia.

References

[1] Rabey M, Poon C, Wray J, Thamajaree C, East R, Slater H. (2015). Pro-nociceptive and anti-nociceptive effects of a conditioned pain modulation protocol in participants with chronic low back pain and healthy control subjects. Man Ther. 2015 Dec;20(6):763-8

Commissioning Editor: Lorimer Moseley;  Editor: Neil O’Connell.

Comments

  1. You obviously put a lot of thought into your work, so if you have something useful to share, then I want to look at it. What could be more relevant than asking another clinican about his approach to the treatment of pain? I’m not here to follow forum rules, I’m here to learn.

    So I read your paper, and you talk about a chronic stress response as a possible cause of fibromyalgia. How did you treat patients with this condition? Don’t you think that prolonged negative emotions can cause that stress?

  2. I’d like to suggest Sapolsky’s contributions to the understanding of stress and biology.

  3. John Quintner says

    Martin, in terms of logical argument, I fail to see how a sensory and emotional experience such as pain can inhibit itself? I don’t think you fell into this trap in your paper but you appear to have done so in the accompanying commentary.

  4. ca c est sur : une douleur violente musculaire ne permet pas de déceler des douleurs dues a des problèmes cardiaques (cas personnel douleurs epaule gauche dues atavorstatine qui ont fait craindre probleme cardiaque en ne permettant pas detection douleur cardiaque)

    John Quintner Reply:

    “This it is certain: an acute muscular pain means that it is difficult to detect if alternately there is a cardiac problem present (personal circumstance of pain in the left shoulder due to atavorstatin which makes one fearful of a cardiac problem – as it makes it difficult to detect cardiac pain).”

    Verdier, is this an accurate translation?

  5. ‘Pro-nociceptive position’ is odd terminology. What he’s referring to is reduced inhibition. Let’s not introduce complications just for the sake of it. Reduced inhibition is caused by concurrent negative emotions.

    https://www.researchgate.net/profile/Katja_Wiech/publication/26252552_Wiech_K_Tracey_I_The_influence_of_negative_emotions_on_pain_behavioral_effects_and_neural_mechanisms_Neuroimage_47_3_987-994/links/53f5b9170cf2fceacc6f57b5.pdf?origin=publication_detail

    There’s still a massive bias preventing clinicians seeing how negative emotions are responsible for disinhibition leading to chronic pain states.

    John Quintner Reply:

    “There’s still a massive bias preventing clinicians seeing how negative emotions are responsible for disinhibition leading to chronic pain states.”

    Is there any scientific evidence that “negative emotions” (and which ones might they be?) can per se alter neurophysiological mechanisms and thereby lead to (i.e. be the cause of) chronic pain states?

    The paper by Weich and Tracey hints at this possibility, but makes the important point that the MRI studies are correlative rather than causal.

    EG Reply:

    I doubt anyone has conducted a trial to stress the shit out of people to see if they develop chronic pain. Ethics committees etc.

    A good paper (not proof): http://www.sciencedirect.com/science/article/pii/S0149763409001614

    There’s also nocebo (not proof but close). Couvade syndrome (not proof, but very close).

    What’s your position? What do you think causes pain? What methods/techniques/drugs/procedures did you used to use? How successful were they?

    John Quintner Reply:

    EG, your questions to me are not relevant to the article and the paper under discussion.

    But in response to your provocative questions, I suggest you might like to read this paper: Lyon P, Cohen ML, Quintner JL. An evolutionary stress-response hypothesis for chronic widespread pain (Fibromyalgia Syndrome). Pain Medicine 2011; 12: 1167-1178.

  6. Chiodo schiaccia chiodo in italian….