One way of understanding pain is more commonly held than the other, but the other is more scientifically accurate. We are thus faced with the prospect that much of society and even many healthcare providers misunderstand the nature of pain.
It’s a provocative prospect, to be sure.
Competing models of pain
Most people, including many healthcare providers, associate pain with tissue damage, a phrase we might use to refer to some form of abnormality of bodily tissue. We might come up with any number of examples -- a cut finger, a burn, or a broken bone, but, of course, there are countless ways we might suffer bodily harm. Generically, we might call such conditions “tissue damage” and we tend to associate it as the cause of pain. Indeed, we tend to think that some form of tissue damage must occur in order for there to be pain. So, if there’s pain, there must be some form of tissue damage that’s causing it.
This way of understanding pain is commonly used in many areas within the field of pain management. Suppose a person develops low back pain and seeks evaluation with a healthcare provider. It’s likely that both the patient and provider will assume that the cause of the back pain is some form of tissue damage in the area of the low back: a muscle strain, a ligament tear, nerve root compression, a disc bulge or herniation, or so forth. Testing, in the form of scans or diagnostic injections, might be pursued in order to identify the tissue damage, which is sometimes further referred to as the “pain generator.” Any number of treatments is subsequently pursued based on the view that some form of tissue damage must be causing the low back pain. Often unspoken, this way of understanding pain thus justifies what healthcare providers go on to do about the pain – various forms of physical therapy, chiropractic care, epidural steroid injections, nerve blocks, and spinal surgeries, all of which are commonly pursued as ways to heal the damaged tissue that must be causing the pain.
In the field of pain management, we refer to this way of understanding the nature of pain as the "Cartesian model." Rene Descartes, a 17th century philosopher and mathematician, was likely not the first person to ever think of pain as occurring in this way, but he was the first to systematically write about it and publish it (Descartes, 1633/2003). This view has had great influence on subsequent generations, so much so, that most people today and many healthcare providers still unquestionably assume it to be true: if there’s pain, there must be some form of tissue damage causing it; so, we have to find the tissue damage and fix it or heal it; once successful in this endeavor, the pain should go away.
The problem with this way of thinking about pain is that, despite how common sense it seems, the empirical evidence doesn’t support it, especially when we use it to understand problems such as back pain.
- Current established guidelines recommend against routine use of MRI or CT scans for low back pain because doing so doesn’t make people better and in some cases makes them worse; in other words, a search for putative tissue damage in the spine doesn’t help when attempting to find ways to have less pain (Cf. Chou, et al., 2011; Flynn, Smith, & Chou, 2011; Koes, et l., 2010).
- The potential identifiable forms of tissue damage that might cause back pain in actuality don't correlate with back pain; if potential forms of tissue damage, such as degenerative conditions of the spine, caused back pain, then we’d expect them to highly correlate with back pain, but they don’t (or at best they are only weakly correlated with back pain) (see, for example, Carragee, et al., 2005; Bogduk, 2012; Videman, et al., 2003).
- Despite varying attempts to prove it over the years, there’s been no demonstrable evidence showing that interventional and spinal surgical procedures are any more than nominally effective (Atlas, et al., 2005; Gibson & Waddell, 2007; Leclaire, et al., 2001; Mirza & Deyo, 2007; Pinto, et al., 2012; van Tulder, et al., 2006; Weinstein, et al., 2006; Weinstein, et al., 2008).
- Few in the field of pain management would argue that back pain isn’t overteated; that is to say, society has seen exponential growth rates in the use of interventional and spinal surgical procedures, but people aren't getting better – they don't return to work faster; they don't reduce their use of opioids; and rates of disability for back pain are increasing, not reducing (Deyo, et al., 2009; Martin, et al., 2009; cf. Nguyen, et al., 2011).
Maybe we need to completely re-think how we think of back pain. Our attempts to provide interventional and surgical therapies to putative "pain generators," or tissue damage, in the spine assumes that because there is pain in the back there must be tissue damage in the back that causes it. However, the widespread and persistent failure of these approaches should suggest that there must be another cause for back pain, something that doesn’t rely on tissue damage to cause it.
And don’t we know already that this must be the case? How else do we make sense of people with back pain who don't exhibit some form of tissue damage that might reasonably account for their pain? Patients with back pain commonly present without objective findings on MRI or CT scans. Just as commonly, patients with back pain present with findings on their sans, but the findings aren't of a type or in a location that might reasonably cause their pain. It’s a common, everyday occurrence. Put together, these two types of back pain patients are likely to be more numerous that the percentage of back pain patients with objective findings that are concordant with their pain.
What often happens in the large percentage of cases in which scans fail to explain the pain is that the legitimacy of the pain is questioned. The basis for such doubt is the Cartesian understanding that pain must have some form of corresponding tissue damage; since there is none in these kinds of cases, their pain is doubted.
Moreover, if the field more fully understood and appreciated the ramifications of the fact that degenerative changes of the spine fail to substantially correlate with pain, we’d have to acknowledge as a field that degenerative changes of the spine as seen on scans simply cannot be the cause of our patients pain as often as we tell them it is – even in cases in which the scans show findings that are of the right type or in the right location to infer a causal role. (Similarly, just as a suspect in a murder case was in fact at the scene of the crime doesn’t mean that he is the murderer.) As such, in a large percentage, if not the majority, of people with back pain, we simply cannot say that the putative tissue damage as seen on scans is the cause of their pain.
How can this be?
This Cartesian view might not be radically inaccurate, but it's likely only accurate in certain circumstances. If I suffer an injury, and so cause some form of tissue damage, such as stepping on a nail, I'll feel pain most of the time. So, in some cases, pain is associated with tissue damage. However, we would commit a logical fallacy (viz., affirming the consequent) to subsequently conclude that all pain must therefore be caused by tissue damage.
We actually have in the field of pain management a competing view of the nature of pain, how it works, and what to do about it. It’s referred to as the “neuromatrix of pain” (Melzack, 1989; Melzack, 1990; Melzack, 1999; Melzack & Loeser, 1978). It explains pain as a function of the central and peripheral nervous system. The nervous system, particularly the brain, is what produces pain. Sometimes, the nervous system produces pain in response to tissue damage, but it can produce pain in response to many other forms of stimuli as well.
In this way, the Cartesian model of pain can be subsumed within the more encompassing neuromatrix model of pain. We might see the Cartesian model of pain as akin to Newtonian physics – Newtonian physics isn’t exactly wrong, but it's only right in certain circumstances and as such it can be subsumed within the larger general relativity theory of physics. Similarly, tissue damage might cause pain, but not all pain is caused by tissue damage.
In the neuromatrix of pain model, we have a scientifically supported understanding of pain that can explain how people have, say, low back pain whether or not they have any identifiable tissue damage in the spine. Consider, for the moment, the wide-ranging and important ramifications of a scientifically accurate model of pain that explains all pain and not just pain for which we can identify a corresponding form of tissue damage:
- Patients would no longer feel the legitimacy of their pain is at stake when, in the majority of cases, no identifiable tissue damage can be found and providers would no longer be at a loss to understand how or why such patients have pain.
- Patients and providers would no longer need to pursue an exhaustive search for putative tissue damage through the use of scans, diagnostic injections, and other assessments when initial findings upon evaluation yield none.
- We could subsequently explain to patients in a convincing way why scans aren't routinely necessary or helpful when it comes to non-specific back pain (i.e., now it simply doesn’t make sense to most patients and some providers because the assumption is that there must be tissue damage otherwise there wouldn’t be pain and so why withhold the use of the technology that might be able to find it?)
- Rates of interventional and surgical procedures could be significantly reduced because we’d no longer be so certain that putative tissue damage must be the "pain generators" of back pain.
- It provides an understandable explanation as to why interdisciplinary chronic pain rehabilitation is persistently shown to be the most effective form of chronic pain management, despite it doing nothing to resolve potential tissue damage that we tend to associate with the cause of pain.
Thus, the wide-scale adoption of the neuromatrix of pain model by patients, their healthcare providers, and society, more generally, would have far-reaching positive effects. In short, we would stop misunderstanding the nature of pain and what we should do about it.
The ICP Mission: Ideas that are Changing Pain
The Institute for Chronic Pain identifies the need to bring our societal understanding of pain into line with the findings of basic pain science of the last fifty years. In so doing, we aim to bring about the afore-mentioned important and necessary changes to the field of chronic pain management. We also understand that to do so it is not sufficient to focus solely on changing provider practice patterns. That is to say, we also need to change how the public at large understands the nature of pain. The guidelines for use of scans in low back pain is a case in point that attests to this fact: if patients don’t understand the basic rationale as to why scans are typically unhelpful in acute low back pain, then they'll continue to expect that the field provides them. No amount of concerted effort on changing provider practice patterns will achieve a change in patient expectations. Instead, we need to explain why a search for putative tissue damage is unhelpful – it’s because in most circumstances back pain isn’t caused by overt tissue damage to the spine and mistakenly believing that it is leads to ineffective overtreatment.
The Institute for Chronic Pain steps into this need for providing understandable, yet scientifically accurate, explanations for the nature of pain and how to best, or most effectively, treat it. We use the internet and social media to proliferate these ideas. Our goal is the widespread adoption of these scientifically accurate ideas about pain, which in turn will change how we treat pain for the better.
To this end, the Institute for Chronic Pain has launched a new webpage on the neuromatrix of pain. Please take look at it and pass it on through your social networks. The more people proliferate these ideas, the more our field of pain management changes for the better.
Atlas, S. J., Keller, R. B., Wu, Y. A., Deyo, R. A., & Singer, D. E. (2005). Long-term outcomes of surgical and non-surgical management of sciatica secondary to a lumbar disc herniation: 10 year results from the Maine Lumbar Spine Study. Spine, 30(8), 927-935.
Bogduk, N. (2012). Degenerative joint disease of the spine. Radiology Clinics of North America, 50(4), 613-628.
Carragee, E. J., Alamin, T. F., Miller, J. L., & Carragee, J. M. (2005). Discographic, MRI and psychosocial determinants of low back pain disability and remission: A prospective study in subjects with benign persistent back pain. Spine Journal, 5(1), 24-35.
Chou, R., Qaseem, A., Owens, D. A., & Shekelle, P. (2011). Diagnostic imaging for low back pain: Advice for high-value health care from the American College of Physicians. Annals of Internal Medicine, 154(3), 181-189.
DesCartes, R. (1633/2003). Treatise of Man. Amherst, NY: Prometheus.
Deyo, R. A., Mirza, S. K., Turner, J. A., & Martin, B. I. (2009). Overtreating chronic back pain: Time to back off? Journal of the American Board of Family Medicine, 22(1), 62-68.
Flynn, T. W., Smith, B., & Chou, R. (2011). Appropriate use of imaging for low back pain: A reminder that unnecessary imaging may do as much harm as good. Journal of Orthopedic & Sports Physical Therapy, 41(11), 838-846.
Gibson J. N., & Waddell, G. (Updated January 6, 2007). Surgical intervention for lumbar disc prolapse. In Cochrane Database of Systematic Reviews, 2007 (2). Retrieved July 4, 2015, from The Cochrane Library, Wiley Interscience.
Koes, B. W., van Tulder, M., Lin, C.-W., Macedo, L. G., McAuley, J., & Maher, C. (2010). An updated overview of clinical guidelines for the management of non-specific back pain in primary care. European Spine Journal, 19(12), 2075-2094.
Leclaire, R., Fortin, L., Lambert. R., Bergeron, Y. M., & Rosignol, M. (2001). Radiofrequency facet joint denervation in the treatment of low back pain: A placebo-controlled clinical trial to assess efficacy. Spine, 26, 1411-1416.
Martin, B. I., Turner, J. A., Mirza, S. K., Lee, M. J., Comstock, B. A., & Deyo, R. A. (2009). Trends in health care expenditures, utilization, health status among US adults with spine problems, 1997-2006. Spine, 34(19), 2077-2084.
Melzack, R. (1999). From the gate to the neuromatrix. Pain, S6, S121-S126.
Melzack, R. (1990). Phantom limbs and the concept of a neuromatrix. Trends in Neurosciences, 13(3), 88-92.
Melzack, R. (1989). Phantom limbs, the self, and the brain (The D. O. Hebb Memorial Lecture). Canadian Psychologist, 30, 1-16.
Melzack, R. & Loeser, J. D. (1978). Phantom body parts in paraplegics: Evidence for a central ‘pattern generating mechanism’ for pain. Pain, 4, 195-210.
Mirza, S. K., & Deyo, R. A. (2007). Systematic review of randomized trials comparing lumbar fusion surgery to nonoperative care for treatment of chronic back pain. Spine, 32, 816-823.
Nguyen, T. H., Randolph, D. C., Talmage, J., Succop, T., & Travis, R. (2011). Long-term outcomes of lumbar fusion among worker's compensation subjects: A historical survey. Spine 36(4), 320-331.
Pinto, R. Z. Maher, C. G., Ferreira, M. L., Hancock, M., Oliveira, V. C., McLachlan, A. J., Koes, B. W., & Ferreira, P. H. (2012). Epidural steroid injections in the management of sciatica: A systematic review and meta-analysis. Annals of Internal Medicine, 157(12), 865-877.
van Tulder, M. W., Koes, B., Seitsalo, S., & Malmivaara, A. (2006). Outcomes of invasive treatment strategies in low back pain and sciatica: An evidence based review. European Spine Journal, 15, S82-S89.
Videman, T., Battie, M., Gibbons, L. E., Maravilla, K., Manninen, H., & Kaprio, J. (2003). Associations between back pain history and lumbar MRI findings. Spine, 28(6), 582-588.
Weinstein, J. N., Tosteson, T. D., Lurie, J. D., et al. (2006). Surgical vs. nonoperative treatment for lumbar disk herniation: The spine patient outcomes research trial (SPORT). Journal of the American Medical Association, 296(20), 2441-2450.
Date of last modification: 7-4-2015
Author: Murray J. McAllister, PsyD