Today is New Zealand’s Waitangi Day ‘Mondayisation’ – the actual day was Saturday 6th Feb. It’s an important day in New Zealand because it’s the day when two completely different nations signed a treaty allowing certain rights between them – and allowed my ancestors to travel from Ireland and England to settle in the country I call my home. Unlike many country’s celebrations of nationhood, Waitangi Day is almost always a time of turbulence, dissension and debate. This is not a bad thing because over the years I think the way in which Maori (Tangata Whenua, or original settlers) and non-Maori settlers (Tangata Tiriti) relate in our country is a fantastic example of living together well. Not perfectly – but certainly in a more integrated way than many other countries where two completely different cultures blend.
Thinking of Waitangi Day, I’m reminded of the way in which the multidimensional model of pain attempts to integrate biological, psychological and social factors to help explain this experience and how such a primitive response to threat can ultimately lead to adaptation and learning – in most cases – or the most profound misery and disability in others.
Like the treaty relationship in New Zealand, there’s much room for discussion and debate as to the relative weight to place on various components of the model. And like the treaty relationship, there are times when each part is accused of dominating and not giving the other/s due credit. Truth, at least to me, is, we need all of us (and all the factors) to integrate – not to become some bland nothing, but to express the components fully.
Just last week I was astonished to find that a clinician thought that I believed low back pain is “psychological”. Absolutely astonished because this has never been my position! While this blog and much of my teaching and reading is around psychological and more recently social factors influencing pain and disability, my position has never been to elevate the influence of these factors over the biological. I suppose I shouldn’t be surprised – it’s hard to deal with the state of play in our understanding of low back pain which finds that many of the assumed causal mechanisms (like disc prolapses, poor “core” muscles, the biomechanics of lifting and so on) just don’t apply. It’s also really difficult to know that so far there are no particular exercise treatments that work more effectively than any other. Cognitive dissonance anyone? Just because these factors are less relevant than presumed does not mean that (a) I think low back pain is psychological and (b) that all biological factors are irrelevant. What it does mean is that we don’t know. I’ll say that again. We. Don’t. Know. Most back pain falls into this “nonspecific” group – and by calling it “nonspecific” we are actually admitting that We. Don’t. Know.
How do people assume that because I point out that we don’t know the causal mechanisms of low back pain but we DO know the critical importance of psychosocial factors on disability associated with low back pain – and the treatments that can mitigate these factors – that I believe back pain is psychological? I think it’s a simple fallacy – some people believe that because a person responds to psychosocial interventions this therefore means their problem is psychological. This is not true – and here are some examples. Exercise (a physical modality) is shown to be an effective treatment for depression. Does this mean depression is a purely biological disorder? Biofeedback provides visual or auditory information related to physical aspects of the body like blood pressure, heart rate, and muscle tension – does this mean that blood pressure is “psychological”? Diabetes management often includes learning to resist the urge, or “urge surf” the impulse to eat foods that increase blood sugar levels – does this mean diabetes is psychological?
Here’s my real position on nonspecific low back pain, which is let me remind you, the most common form of low back pain.
Causes – not known (Golob & Wipf, 2014), risk factors for onset are mainly equivocal but one study found the major predictor of an onset was – prior history of low back pain, with “limited evidence that the combination of postural risk factors and job strain is associated with the onset of LBP” (Janwantanakul, Sitthipornvorakul, & Paksaichol, 2012), exercise may prevent recurrence but mechanisms of LBP remain unclear (Macedo, Bostick and Maher, 2013), while subgroup analysis carried out by therapists were “underpowered, are only able to provide exploratory or insufficient findings, and have rather poor quality of reporting” (Mistry, Patel, Wan Hee, Stallard & Underwood, 2014).
My take from this brief review? The mechanisms presumed to be involved in nonspecific low back pain are unknown.
Treatments – mainly ineffective but self-management provides small effects on pain and disability (moderate quality) (Oliveira, Ferreira, Maher, Pinto, Refshauge & Ferreira, 2012), “the evidence on acupuncture for acute LBP is sparse despite our comprehensive literature search” (Lee, Choi, Lee, Lee, Shin & Lee, 2013), no definitive evidence supports the use of orthoses for spine pain (Zarghooni, Beyer, Siewe & Eysel, 2013), acetaminophen is not effective for pain relief (Machado, Maher, Ferreira, Pinheiro, Lin, Day et al, 2015), and no specific exercises are better than any other for either pain relief or recovery – not even motor control exercises (Saragiotto, Maher, Yamato, Costa et al, 2016).
My take from this set of references is that movement is good – any movement, but no particular form of exercise is better than any other. In fact, the main limitation to exercise is adherence (or actually continuing exercising after the pain has settled).
The factors known to predict poor recovery are pretty clear – catastrophising, or thinking the worst (Kim, Cho, Kang, Chang, Lee, & Yeom, 2015), avoidance (usually arising from unhelpful beliefs about the problem – see commentary by Schofferman, 2015), low mood – which has also been found to predict reporting or treatment seeking of low back pain (see this post from Body in Mind, and this one).
What can I take from all of this? Well, my view is that because psychosocial factors exert their influence at multiple levels including our nervous system (see Borkum, 2010), but also our community understanding of what is and isn’t “illness” (Jutel, 2011) and who to see and what to do about it, the problem of nonspecific low back pain is one of the purest forms of an integrated biopsychosocial and multifactorial health concern in human life. I therefore rest my case: nonspecific low back pain is not psychological, but neither is it biomechanical or biological only. It is a biopsychosocial multifactorial experience to which humans are prone.
The best we can do with our current knowledge base is (1) limit and avoid the use of nocebic language and attempts to explain low back pain via biomechanical or muscle control mechanisms, (2) be honest about the likelihood of low back pain recurring and our treatments essentially doing very little, and (3) encourage return to normal activity by doing normal activity including exercise. Being honest about the state of play in our knowledge is a good starting point for better understanding – sounds a lot like race relations, doesn’t it?
Borkum, J. M. (2010). Maladaptive cognitions and chronic pain: Epidemiology, neurobiology, and treatment. Journal of Rational-Emotive & Cognitive Behavior Therapy, 28(1), 4-24. doi:http://dx.doi.org/10.1007/s10942-010-0109-x
Golob, A. L., & Wipf, J. E. (2014). Low back pain. Medical Clinics of North America, 98(3), 405-428.
Janwantanakul, P., Sitthipornvorakul, E., & Paksaichol, A. (2012). Risk factors for the onset of nonspecific low back pain in office workers: A systematic review of prospective cohort studies. Journal of Manipulative & Physiological Therapeutics, 35(7), 568-577.
Jutel, A. (2011). Classification, disease, and diagnosis. Perspectives in Biology & Medicine, 54(2), 189-205.
Kim, H.-J., Cho, C.-H., Kang, K.-T., Chang, B.-S., Lee, C.-K., & Yeom, J. S. (2015). The significance of pain catastrophizing in clinical manifestations of patients with lumbar spinal stenosis: Mediation analysis with bootstrapping. The Spine Journal, 15(2), 238-246. doi:http://dx.doi.org/10.1016/j.spinee.2014.09.002
Lee, J. H., Choi, T. Y., Lee, M. S., Lee, H., Shin, B. C., & Lee, H. (2013). Acupuncture for acute low back pain: A systematic review. Clinical Journal of Pain, 29(2), 172-185.
Macedo, L. G., Bostick, G. P., & Maher, C. G. (2013). Exercise for prevention of recurrences of nonspecific low back pain. Physical Therapy, 93(12), 1587-1591.
Machado, G. C., Maher, C. G., Ferreira, P. H., Pinheiro, M. B., Lin, C.-W. C., Day, R. O., . . . Ferreira, M. L. (2015). Efficacy and safety of paracetamol for spinal pain and osteoarthritis: Systematic review and meta-analysis of randomised placebo controlled trials. BMJ, 350, h1225.
Mistry, D., Patel, S., Hee, S. W., Stallard, N., & Underwood, M. (2014). Evaluating the quality of subgroup analyses in randomized controlled trials of therapist-delivered interventions for nonspecific low back pain: A systematic review. Spine, 39(7), 618-629.
Oliveira, V. C., Ferreira, P. H., Maher, C. G., Pinto, R. Z., Refshauge, K. M., & Ferreira, M. L. (2012). Effectiveness of self-management of low back pain: Systematic review with meta-analysis. Arthritis care & research, 64(11), 1739-1748.
Saragiotto Bruno, T., Maher Christopher, G., Yamato Tiê, P., Costa Leonardo, O. P., Menezes Costa Luciola, C., Ostelo Raymond, W. J. G., & Macedo Luciana, G. (2016). Motor control exercise for chronic non-specific low-back pain. Cochrane Database of Systematic Reviews, (1).
Schofferman, J. A. (2015). Commentary on the significance of pain catastrophizing in clinical manifestations of patients with lumbar spinal stenosis: Mediation analysis with bootstrapping. The Spine Journal, 15(2), 247-248. doi:http://dx.doi.org/10.1016/j.spinee.2014.11.003
Zarghooni, K., Beyer, F., Siewe, J., & Eysel, P. (2013). The orthotic treatment of acute and chronic disease of the cervical and lumbar spine. Deutsches Arzteblatt International, 110(44), 737-742.