Teaching people about pain – why do we keep beating around the bush

A frank approach to interpersonal communication brings with it some challenges, but having to dig oneself out of a hole, created by strategically avoiding the truth, is not one of them. This frank approach is well suited to science – the scientific process requires us to pursue and report the truth, the whole truth and nothing but the truth. We do not tend to avoid aspects of the truth because we think that they are too hard for people to understand; for example, we do not avoid the amazing truth that the brain constructs visual experience from the information available to it, and instead suggest that the eyes themselves actually create visual experience and send the visual experience to the brain to be registered; we do not suggest that the ears capture words and bird-calls and racing cars and send those sounds to the brain to be registered. We tend to endorse the complexity of the brain and its fundamental role in what we experience. Unless, of course, we are talking about pain.

Some 25 years ago, Patrick Wall, as frank a communicator as any, lamented the trend towards beating around the bush when it comes to pain: “The labeling of nociceptors as pain fibers was not an admirable simplification, but an unfortunate trivialization under the guise of simplification” [1]. Of course, equating pain to activity in nociceptors is seductive – nociception and pain seem so tightly coupled. However, are nociception and pain really so tightly coupled? This issue was actually settled a couple of decades ago – there is not an isomorphic relationship between pain and nociception, nor between pain and tissue damage [2]. A very large amount of research has explored the multifactorial nature of pain (see [3] for a clinic-friendly review). Modulators broadly fit into one of three categories: prioritization, meaning and transmission/processing. Prioritization depends on the survival value of a nociceptive stimulus. Observational data abound; for example, the extensive work with military and civilian injuries – the soldier feels little pain until he is safe behind lines [4]. Experimental data have corroborated this – noxious stimuli do not hurt in cases of extreme air hunger [5] – and the pain threshold is higher after a bout of startlingly loud noises [6].

The second category – meaning – is, in my view, the most important to those of us working in the clinical pain sciences. Meaning is a very potent modulator of the relationship between nociception and pain. Indeed, one might argue that meaning is the critical determinant of pain, because if a nociceptive input is not evaluated by the brain as reflecting a threat to body tissue, pain would clearly be an erroneous output, serve no survival function and offer no evolutionary advantage. Again, anecdotal data abound – most strikingly, there are religious or cultural practices that involve severe noxious input, but no pain is reportedly experienced – and experimental data have corroborated this: a very cold noxious stimulus hurts more if there are explicit [7] or implicit [8] cues that provide credible information to suggest that the very cold stimulus is actually very hot, which would be more dangerous to body tissue.

The third category – transmission/processing – refers to both the well-established state-dependent functioning of nociceptive pathways and real-time modulation of transmission and processing by, for example, expectation [9]. Real-time modulation can involve neurally, neurochemically or humorally driven alteration of the response profile of neurones within the nociceptive neuraxis [10].

So, the mislabeling of nociceptors as pain fibers was indeed a trivialization, but was it really that unfortunate? I contend that one need only look at the huge burden of chronic pain to uphold a resounding ‘yes’. Chronic pain is terribly costly to our societies – approximately US$1500 per person per year in the USA [101] – and to the individual sufferers of pain, who often descend into a spiral of increasing economic, social and personal disadvantage. The evidence that tissue pathology does not explain chronic pain is overwhelming (e.g., in back pain [11], neck pain [12] and knee osteoarthritis [13]). Yet we continue to avoid the truth that tissue damage, nociception and pain are distinct. I would go so far as to suggest that even the use of these erroneous terms – pain receptors, pain fibers and pain pathways – leaves the patient with chronic pain feeling illegitimate and betrayed, and leaves the rehabilitation team lacking credibility when they look beyond the tissues for a way to change pain.

Generally speaking, however, are these issues usually more than just semantics? Can one argue that it might be unhelpful to simplify things when we are talking about chronic pain, but it is fine when we are talking about acute pain? This suggestion requires us to adopt a different understanding of biology once someone ‘goes chronic’. This is problematic, not least because those in chronic pain first had acute pain, and to change our story once they are chronic might give the distinct impression that we are clutching at straws. Indeed, by the time people progress from acute to chronic pain, our previous avoidance of the truth – our unfortunate trivialization – has dug a very big hole from which it is difficult to climb out.

To be continued…

Previously published in: Moseley, G. (2012). Teaching people about pain: why do we keep beating around the bush? Pain Management, 2 (1), 1-3 DOI: 10.2217/pmt.11.73

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 hereDownloadable PDFs here.

References

[1] Wall P, McMahon S. The relationship of perceived pain to afferent nerve impulses. Trends Neurosci. 9(6), 254–255 (1986).

[2] Wall PD, McMahon SB. Microneuronography and its relation to perceived sensation. A critical review. Pain 21(3), 209–229 (1985).

[3] Butler D, Moseley GL. Explain Pain. NOI Group Publishing, Australia (2003).

[4] Beecher H. Relationship of the significance of the wound to the pain experience. JAMA 161(17), 1609–1613 (1956).

[5] Banzett RB, Gracely RH, Lansing RW. When it’s hard to breathe, maybe pain doesn’t matter. Focus on “Dyspnea as a noxious sensation: inspiratory threshold loading may trigger diffuse noxious inhibitory controls in humans”. J. Neurophysiol. 97(2), 959–960 (2007).

[6] Meagher MW, Rhudy JL. Noise stress and human pain thresholds: divergent effects in men and women. J. Pain 2(1), 57–64 (2001).

[7] Arntz A, Claassens L. The meaning of pain influences its experienced intensity. Pain 109, 20–25 (2004).

[8] Moseley GL, Arntz A. The context of a noxious stimulus affects the pain it evokes. Pain 133, 64–71 (2007).

[9] Keltner JR, Furst A, Fan C, Redfern R, Inglis B, Fields HL. Isolating the modulatory effect of expectation on pain transmission: a functional magnetic resonance imaging study. J. Neurosci. 26(16), 4437–4443 (2006).

[10] Ren K, Dubner R. Enhanced descending modulation of nociception in rats with persistent hindpaw inflammation. 18 J. Neurophysiol. 76(5), 3025–3037 (1996).

[11] van Tulder MW, Assendelft WJ, Koes BW, Bouter LM. Spinal radiographic findings and nonspecific low back pain. A systematic review of observational studies. Spine 22(4), 19 427–434 (1997).

[12] Peterson C, Bolton J, Wood AR, Humphreys BK. A cross-sectional study correlating degeneration of the cervical spine with disability and pain in United Kingdom patients. Spine 28(2), 129–133 (2003). 20

[13] Link TM, Steinbach LS, Ghosh S et al. Osteoarthritis: MR imaging findings in different stages of disease and correlation with clinical findings. Radiology 226(2), 373–381 21 (2003).

[101] Website: Health, United States, 2010, with special feature on death and dying. www.cdc.gov/nchs/data/hus/hus10.pdf