Do We Tend to Misunderstand the Nature of Pain?

We live in an interesting time within the field of pain management. We literally have two competing ways of understanding the nature of pain – what it is and how it works and what to do about it. 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 Cartesian Model of Painphrase 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. 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 of painneuromatrix 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.

References

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 neuromatrixPain, S6, S121-S126.

Melzack, R. (1990). Phantom limbs and the concept of a neuromatrixTrends 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.

Weinstein, J. N., Lurie, J. D., Tosteson, T. D., et al. (2008). Surgical vs. nonoperative treatment for lumbar disc herniation: Four-year results for the spine patient outcomes research trial (SPORT)Spine, 33, 2789-2800.

Author: Murray J. McAllister, PsyD

Date of last modification: 7-4-2015

Is Degenerative Disc Disease Painful?

‘Correlation doesn’t imply causation.’ It’s a commonly expressed caution in the health sciences. What it means is that things can tend to go together without necessarily causing each other. The classic example that statistic professors like to give is that air conditioner use is significantly correlated with street crime. Does the use of air conditioners cause street crime? No, of course, not and yet they do tend to go together. It’s actually only because they both tend to occur in the summer. When it’s hot outside, it’s true that people tend to use their air conditioners and it’s also true that people tend to loiter outside in the city, getting into trouble more often than in the cold winter months when people tend to stay indoors. With the example, we can see that just because things tend to go together they don’t also always cause each other.

What about things that hardly go together or things that don’t go together at all? Could we say that low levels of correlation or an altogether lack of correlation imply causation? On the face of it, it seems absurd to think that lack of correlation or even minimal correlation might imply causation. Who would think that A causes B when A and B have no relationship to one another or only a minimal association with one another? That inference, however, is exactly what we assume when we think that degenerative disc disease causes chronic back or neck pain.

The logic of correlational studies of degenerative disc disease and chronic spine pain

Degenerative disc disease is a common explanation for chronic back or neck pain. Degenerative disc disease is a general phrase that refers to a number of conditions or changes of the spine, such as loss of disc height, disc bulges, annular tears, disc herniations, endplate changes, neuroforaminal and spinal canal stenosis, among others. Healthcare providers typically identify their occurrence with either X-ray, CT or MRI scans. When these tests identify degenerative disc disease in the spine of someone experiencing chronic back or neck pain, many healthcare providers and their patients consider that the degenerative disc disease is the cause of the chronic pain. In other words, they believe that the degenerative disc disease is painful.

Healthcare providers and their patients commonly justify particular types of treatment with the notion that degenerative disc disease is causing chronic back or neck pain. Spine surgery and interventional pain procedures, in particular, but also certain types of physical therapy, all attempt to reduce pain by modifying specific types of degenerative changes of the spine. Again, the underlying justifying belief is that such degenerative changes of the spine are painful.

How valid is this justification? In other words, how true is it that degenerative disc disease causes chronic back or neck pain?

The question is actually tricky to answer, especially if we want to show that it is in fact true. Theoretically, the best way to answer it would be to run a true experiment, where we induce various degenerative changes to the spine in a number of people and see whether they have pain in the back or neck (wherever the degenerative change was induced). However, we don’t know how to make degenerative changes to the spine, at least not exactly as they occur naturally. Additionally, even if we did know how, there would be all sorts of ethical problems in producing degenerative disc disease in human subjects. For instance, we don’t know how to reverse it and so we’d be inducing permanent damage to people. Because of these challenges, we don’t tend to perform true experiments when looking at the relationship between degenerative disc disease and chronic neck and back pain.

Instead, we generally rely on a different form of research in the scientific study of chronic pain – correlational research. In correlational research, we measure certain variables, such as the occurrence of degenerative disc disease and back or neck pain, and see whether they tend to go together. If two things, such as degenerative disc disease and pain, are highly correlated (i.e., they tend to go together almost always), we can at least say that one may cause the other. As we discussed in the introduction of this piece, though, we cannot say with confidence that there is a causal relationship when two things are highly correlated. There may be other factors that cause the two to occur together all the time (i.e., think of the air conditioner use and street crime example). Nonetheless, it is helpful to see whether they correlate together and what the strength of the correlation is. The reason is that if they don’t correlate at all or if the correlation is very weak, then we can say with confidence that they don’t cause each other.

To understand, we need to look at the following reasoning: when one thing causes another thing, they must occur together in some demonstrable way; if, however, when one thing occurs, another thing may or may not occur, they have no relationship to each other and so we cannot say that there is a causal relationship. A causal relationship presupposes a correlational relationship. Now, as we have said before, a correlational relationship is not enough to demonstrate a causal relationship, but to have a causal relationship, there at least has to be a correlational relationship. We have to at least be in the right ballpark, as it were. Without a correlational relationship, though, we can say with much greater confidence that we are not even in the right (i.e., causal) ballpark. In other words, if we find no correlation, we can safely assert that there is no causal relationship.

A similar, albeit slightly different logic holds with weak correlations – the situation in which two things go together in some minimal ways. With such correlations, we can say that there may be a causal relationship between the variables, just as we said with strong correlations, but we can’t know for sure because correlation doesn’t imply causation. Now, with weak correlations, however, we can go a step further. We can assume that even if there was a causal relationship between the two variables, we know that there has to be more to the picture than simply the two weakly correlated variables. In other words, there has to be additional causal variables coming into play, because if there weren’t the correlation would have to be strong. The weak correlation, even in cases where we might assume a causal relationship, shows that the variable is only part of the cause – and only a small part at that.

It would be helpful to take an example. Let’s suppose that we did a study of the relationship between the presence of eating utensils and cookware in the kitchen on the one hand and how much food people ate on the other hand. In a sample of 1,000 people, we measured a) the extent to which they had eating utensils and cookware in the kitchen and b) how much they ate on average over the course of a month. Let’s further suppose we found a weak, statistically significant, relationship between our two variables of interest. It’s a fantastical example, of course, but we might see how it could be true: the presence of eating utensils and cookware could play some small role in how much you ate on average – if you don’t have a way to prepare and eat food, it could affect how much you eat. However, we can also immediately see that there’s more to the picture in terms of what goes into the fact of how much food people eat. The extent to which you have ways to prepare and eat food are not the only variables that can lead to eating. People can eat raw foods; they can eat with their hands; they can buy prepared foods in the grocery store, delis, and fast food restaurants; they can go out to eat in sit-down restaurants; and so on. Personal characteristics of the people can also play a role: how hungry they are or how much stress they are under or how busy they are can also affect how much people eat – even in people who don’t have adequate means to prepare food. In all these ways, we can see that a weak, statistically significant, correlational relationship cannot explain the whole nature of the relationship between two variables, even when we assume that they are in some ways causally related.

As we will see in the following review of the correlational research on degenerative disc disease and chronic back or neck pain, degenerative changes of the spine fit into one of these two categories: they either have no relationship at all with chronic back or neck pain, or they are only weakly related to chronic back or neck pain. As such, we can conclude with confidence one of two things, depending on the type of degenerative disc disease we are discussing. First, in the case where research repetitively shows no correlational relationship between certain types of degenerative disc disease and chronic back or neck pain, these particular types of degenerative changes do not cause pain, despite the common belief that they do. Second, in the case where research repetitively shows a weak, statistically significant, correlational relationship between certain types of degenerative disc disease and chronic back or neck pain, these particular types of degenerative disc disease may play some role in producing pain, but we know that it is only a minimal role, even if we assume that the correlation reflects a causal relationship. In other words, the weak correlation between certain types of degenerative disc disease and pain shows that the lion’s share of what’s causing the pain is something else entirely. This statement too stands in stark contrast to the common belief that degenerative disc disease is the predominant cause of chronic back or neck pain.

Let’s, then, review the correlational research on the relationship between the different types of degenerative disc disease and chronic back or neck pain.

Correlation (or lack thereof) between pain and degenerative disc disease

In a review of early studies, van Tulder, at al., (1997) found weak significant associations between back pain and disc space narrowing, osteophytes, and sclerosis, with odds ratios in the range of 1.2-3.3. Other degenerative changes, such as spondylosis, spondyolisthesis, and kyphosis had no relationship to back pain.

In their review of the literature on the natural history and clinical significance of disc herniation, Grande, Maus, and Carrino (2012) conclude that there is no relationship between any characteristics of disc herniation, including size or severity, and subsequent symptoms of patients.

Mitra, Cassar-Pullicino and McCall (2004) found no relationship between evidence of an annular tear in the disc and pain.

Jarvinen, et al., (2015) found no significant correlation between Modic 1 or Modic 2 changes and low back pain.

de Schepper, et al., (2010) studied the relationship between osteophytes, disc space narrowing, and low back pain. They found that disc space narrowing, especially, at more than one level, was most significantly related to low back pain, but only weakly, with an odds ratio of 2.4.

In a more statistically oriented review, Chou, et al, (2011), systematically searched the literature and combined studies to determine the odds ratio for having lumbar degenerative changes and chronic low back pain. They found a significant, yet weak, association between the two. The range for the odds ratio was between 1.8-2.8.

Livshits, et al., (2011) found a significant relationship between all degenerative changes of the spine and pain with an odds ratio of 3.2.

In a study published after the Chou, et al. findings, Nemoto, et al., (2012) found a significant correlation between vertebral osteophytes and low back pain, but the odds ratio was a little greater at 3. In contrast to the de Schepper, et al, study cited above, they found no correlation between disc space narrowing and back pain.

All these data are what likely led Bogduk (2012), one of the founding fathers of interventional pain management, to conclude, “Degenerative changes [of the spine] lack any significant correlation with spinal pain.”

These findings are also similar to the relationship between degenerative disc disease and pain related disability. Quack, et al., (2007) found either no relationship or only weak correlations between lumbar degenerative changes and mobility. Sirvanci, et al., (2008), found no significant relationship between lumbar spinal stenosis and perceived disability, as measured by the Oswestry Disability Index. Lohman, et al., (2006) found no relationship between spinal stenosis and pain or scores on the Oswestry Disability Index. Remes, et al., (2005) in a cohort of patients who underwent fusion for spondylolisthesis twenty years ago, found no relationship between lumbar degenerative changes and the same measure of disability. Similarly, looking at a number of biological and lifestyle factors, Wilkens, et al., (2013) found that degenerative changes as found on imaging failed to correlate with perceived disability one year later as measured by the Roland-Morris Disability Questionnaire.

Conclusion

This review of the literature shows that the various types of degenerative disc disease either have no relationship to pain and disability or only a weak correlation to pain and disability. What this means is that degenerative disc disease is likely not painful. At best, it plays a minimal role in the cause of chronic back or neck pain. The true cause of chronic back or neck pain must be something else entirely.

For more information on degenerative disc disease, please see the previous blog post and the Institute for Chronic Pain content page on degenerative disc disease.

References

Bogduk, N. (2012). Degenerative joint disease of the spine. Radiology Clinics of North America, 50(4), 613-628. doi: 10.1016/j.rcl.2012.04.012

Chou, D., Semartzis, D., Bellabarba, C., Patel, A., Luk, K., Kisser, J. M., & Skelly, A. C. (2011). Degenerative magnetic resonance imaging changes in patients with chronic low back pain: A systematic review. Spine, 36, S43-S53. doi: 10.1097/BRS.0b013e31822ef700

Del Grande, F., Maus, T. P., & Carrino, J. A. (2012). Imaging the intervetebral disk: Age-related changes, herniation, and radicular pain. Radiology Clinics of North America, 50(4), 629-649. doi: 10.1016/j.rcl.2012.04.012

de Schepper, E., Damen, J., van Meurs, J. B., Ginai, A. Z., Popham, M., Hofman, A., Koes, B. W., & Bierma-Zeinstra, S. M. (2010). The association between lumbar disc degeneration and low back pain: The influence of age, gender, and individual radiographic features. Spine, 25(5), 531-536. doi: 10.1097/BRS.0b013e3181aa5b33

Jarvinen, J., Karppinen, J., Niinimaki, J., Haapea, M., Gronblad, M., Luoma, K., & Rinne, E. (2015). Associations between changes in lumbar Modic changes and low back symptoms over a two year period. BMC Musculoskeletal Disorder, 16, 98. doi: 10.1186/s12891-015-0540-3

Livshits, G., Popham, M., Malkin I., Sambrook, P. M., MacGregor, A. J., Spector, T., & Williams, F. M. (2011). Lumbar disc degeneration and genetic risk factors are the main risk factors for low back pain in women: The UK twin spine study. Annals of Rheumatic Disease, 70(10), 1740-1745. doi: 10.1136/ard.2010.137186

Lohman, C. M., Tallroth, K., Kettunen, J. A., & Lindgren, K. (2006). Comparison of radiologic signs and clinic symptoms of spinal stenosis. Spine, 31(16), 1834-1840.

Maus, T. (2010). Imaging the back pain patient. Archives of Physical Medicine and Rehabilitation, 21(4), 725-766. doi: 10.1016/j.pmr.2010.07.004

Mitra, D., Cassar-Pullicino, V. N., & McCall, I. W. (2004). Longitudinal study of high intensity zones on MR of lumbar intervetebral discs. Clinical Radiology, 59(11), 1002-1008.

Nemoto, O., Kitada, A., Naitou, S., Tsuda, Y., Matsukawa, K., & Ukegawa, Y. (2012). A longitudinal study for incidence of low back pain and radiological changes of lumbar spine in asymptomatic Japanese military young adults. European Spine Journal, 22, 453-458. doi: 10.1007/s00586-012-2488-4

Quack, C., Schenk, P., Laeubil, T., Spillmann, S., Hodler, J., Michel, B. A., & Klipstein, A. (2007). Do MRI findings correlate with mobility tests? AN explorative analysis of the test validity with regard to structure. European Spine Journal, 16(6), 803-812.

Remes, V. M., Lamberg, T. S., Tervahartiala, P. O., Helenius, I. J., Osterman, K., Schlenzka, D., Yrjonen, T., Seitsalo, S., & Poussa, M. S. (2005). No correlation patient outcome and MRI findings 21 years after posterior or posterolateral fusion for isthmic spondylolisthesis in children and adolescents. European Spine Journal, 14(9), 833-842.

Sirvanci, M., Bhatia, M., Ganiyusufoglu, K. A., Duran, C., Tezer, M., Ozturk, C., Aydogan, M., & Hamzaoglu, A. (2008). Degenerative lumbar spinal stenosis: Correlation with Oswestry Disability Index and MR imaging. European Spine Journal, 17(5), 679-685. doi: 10.1007/s00586-008-0646-5

van Tulder, M. W., Assendelft, W. J., Koes, B. W., & Bouter, L. M. (1997). Spine, 22(4), 427-434.

Wilkens, P., Scheel, I. B., Grundes, O., Hellum, C., & Storheim, K. (2013). Prognostic factors of prolonged disability in patients with chronic low back pain and lumbar degeneration in primary care: A cohort study. Spine, 38(1), 65-74. doi: 10.1097/BRS.0b013e318263bb7b

Author: Murray J. McAllister, PsyD

Date of last modification: 5-31-2015

From Degenerative Disc Disease to Central Sensitization: A Paradigm Shift

Thomas Kuhn, a historian of science, popularized the notion of a scientific paradigm in the second half of the 20th century and since then almost every significant change in a field of study gets characterized as a “paradigm shift.” So, it is a bit of a cliché to talk of the “paradigm shift” that is going on in the field of chronic pain management. Nonetheless, it is true.

We are actually witnessing it happening. The field of chronic pain management is undergoing a change in both how we understand the nature of chronic pain and how we subsequently treat it. While observable with any number of chronic pain conditions, this paradigmatic shift is most clear in the case of chronic back pain.

For the last twenty to thirty years, we have understood chronic back pain as a symptom of an underlying disease process of the spine called degenerative disc disease. This conceptualization has led to a common view of chronic back pain as a long-lasting orthopedic injury or condition. In the last ten years or so, a competing explanation for chronic back pain has begun to take hold. It is the notion that chronic pain is a nervous system condition, not an orthopedic condition. The condition is called “central sensitization.” It is the understanding that chronic pain results when the nervous system, including the brain, becomes stuck in a persistent state of reactivity, which leads the nervous system to become highly sensitive. The nervous system gets stuck, as it were, in a ‘hair trigger’ mode.

CNSThese competing ways of understanding the nature of chronic pain explains the occurrence of chronic back pain symptoms differently. Take, for example, symptoms of back pain that occur with normal movements, like walking, standing, leaning over, sitting down or getting up from a chair. Pain with simple movements such as these is often perplexing to the patient and their loved ones: these kinds of movements shouldn’t be painful, but they are to many patients with chronic back pain.

Those who uphold the view that chronic back pain is the result of degenerative disc disease would make sense of these symptoms by considering the normal movements as somehow aggravating the underlying degenerative changes of the spine. If the onset of these symptoms occurred slowly over time, they might posit that normal movements have become painful because the degenerative changes of the spines are progressively degenerating.

Those who uphold the view that chronic back pain is due to central sensitization would make sense of the symptom by understanding that the nervous system has become stuck in a persistent state of reactivity. This persistent reactivity has subsequently made the nervous system highly sensitive, so sensitive that even normal activities, such as those listed above, are painful. Indeed, the sensitivity can be so great that even simple pressure, such as touch and hugs, can increase pain and mild bumps to the painful area can send patients through the roof.

A number of factors are leading this change in our understanding of the nature of chronic back pain:

  • The proliferation of scientific studies and publications linking the brain and the rest of the nervous system to the onset and maintenance of chronic pain (see, for examples, Apkarian, Baliki, & Geha, 2009; Baliki, et al., 2006; Chapman, Tuckett, & Song, 2008; Curatolo, Arendt-Nielsen, & Petersen-Felix, 2006; Woolf, 2011).
  • The explanatory nature of central sensitization explains not only the chronicity of pain, but also its psychosocial aspects, such as excessive fatigue, insomnia, poor concentration and short-term memory, gastrointestinal upset, anxiety, and depression (Meeus & Nijs, 2007; Wieseler-Frank, Maier, & Watkins, 2005; Yunus, 2007).
  • Numerous studies show consistent findings that chronic pain rehabilitation, an interdisciplinary therapy that focuses on down-regulating the nervous system, is the most effective form of chronic pain management (see, for examples, Gatchel & Okifuji, 2006; Turk, 2002).
  • In contrast, the explanation that degenerative disc disease is the cause of chronic back pain leads patients into the mistaken belief that their spines are fragile and inevitably going to worsen. This set of beliefs further lead patients to respond with behaviors that are more appropriate to acute injuries — rest, inactivity, and extended use of narcotic pain relievers. When done over time, these behaviors can lead to fear-avoidance, de-conditioning, and disability (Leeuw, et al., 2007; Vlaeyen & Linton, 2000).
  • Numerous studies show consistent findings that surgical and interventional procedures are largely, though not wholly, ineffective (Gibson & Waddell, 2007; Leclaire, et al., 2001; Mirza & Deyo, 2007; van Tulder, et al., 2006; van Wijk, et al., 2005; Weinstein, et al., 2006; Weinstein, et al., 2008). These procedures presume chronic pain to be the result of an orthopedic condition, specifically degenerative disc disease.
  • While degenerative changes of the spine have some relation to pain, the correlation between such changes and pain is weak to modest, at best (Endean, Palmer, & Coggon, 2011). In the case of chronic back pain, these low correlations indicate that much is left unexplained when attributing the cause to degenerative changes of the spine.
  • Numerous studies show consistent findings that degenerative disc disease is neither inevitably degenerative nor a disease (see, for examples, Carragee, et al., 2006; Hutton, et al., 2011; Jarvik, et al., 2005; Jensen, et al., 1994; Matsubara, et al., 1995; Takatalo, et a., 2009).

Knowledge in science advances when both different investigators consistently come to similar findings and, subsequently, a shift occurs in how the community of stakeholders sees and understands a particular phenomenon. In chronic pain management, the sheer numbers of data are all pointing to the same conclusion: the notion of degenerative disc disease does not explain the majority of the variance of chronic back pain symptoms, but rather the notion of central sensitization does. In other words, chronic back pain is a nervous system condition, not an orthopedic condition. Presently, we are witnessing this shift in our paradigmatic understanding of chronic back pain.

 

References

Apkarian, A. V., Baliki, M. N., & Geha, P. Y. (2009). Towards a theory of chronic pain. Progress in Neurobiology, 87, (2), 81-97.

Baliki, M. N., Chialvo, D. R., Geha, P. Y., Levy, R. M., Harden, R. N., Parrish, T. B., & Apkarian, A. V. (2006). Chronic pain and the emotional brain: Specific brain activity associated with spontaneous fluctuations of intensity of chronic back pain. Journal of Neuroscience, 26, 12165-12173,

Carragee, E., Alamin, T., Cheng, I., Franklin, T., & Hurwitz, E. (2006). Does minor trauma cause serious low back illness? Spine, 31, 2942-2949.

Chapman, C. R., Tuckett, R. P., & Song, C. W. (2008). Pain and stress in a systems perspective: Reciprocal neural, endocrine and immune interactions. Journal of Pain, 9, 122-145.

Curatolo, M., Arendt-Nielsen, L., & Petersen-Felix, S. (2006). Central hypersensitivity in chronic pain: Mechanisms and clinical implications. Physical Medicine and Rehabilitation Clinics of North America, 17, 287-302.

Endean, A., Palmer, K. T., & Coggon, D. (2011). Potential of MRI findings to refine case definition for mechanical low back pain in epidemiological studies: A systematic review. Spine, 36, 160-169.

Jarvik, J. G., Hollingworth, W., Heagerty, P. J., Haynor, D. R., Boyko, E. J., & Deyo, R. A. (2005) Three-year incidence of low back pain in an initially asymptomatic cohort. Spine, 30, 1541-1548.

Jensen, M. C., Brant-Zawadzki, M. N., Obuchowski, N., Modic, M. T., Malkasian, D., Ross, J. S. (1994). Magnetic resonance imaging of the lumbar spine in people without back pain. New England Journal of Medicine, 331, 69-73.

Gatchel, R., J., & Okifuji, A. (2006). Evidence-based scientific data documenting the treatment and cost-effectiveness of comprehensive pain programs for chronic non-malignant pain. Journal of Pain, 7, 779-793.

Gibson J. N., & Waddell, G. (Updated January 6, 2007). Surgical intervention for lumbar disc prolapse. In Cochrane Database of Systematic Reviews, 2007 (2). Retrieved November 25, 2011, from The Cochrane Library, Wiley Interscience.

Hutton, M. J., Baker, J. H., & Powell, J. M. (2011). Modic vertebral body changes: The natural history as assessed by consecutive magnetic resonance imaging. Spine, 36, 2304-2307.

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.

Leeuw, M., Goossens, M. E., Linton, S. J., Crombez, G., Boersma, K., & Vlaeyen, J.W. (2007). The fear-avoidance model of musculoskeletal pain: Current state of scientific evidence. Journal of Behavioral Medicine, 30, 77-94.

Matsubara, Y., Kato, F., Mimatsu, K., Kajino, G., Nakamura, S., & Nitta, H. (1995). Serial changes on MRI in lumbar disc herniations treated conservatively. Neuroradiology, 37, 378-383.

Meeus M., & Nijs, J. (2007). Central sensitization: A biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome. Clinical Journal of Rheumatology, 26, 465-473.

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.

Takatalo, J., Karppinen, J., Niinimaki, J., Taimela, S., Nayha, S., Jarvelin, M. R., Kyllonen, E., Tervonen, O. (2009). Prevalence of degenerative imaging findings in lumbar magnetic imaging among young adults. Spine, 34, 1716-1721.

Turk, D. C. (2002). Clinical effectiveness and cost-effectiveness of treatments for patients with chronic pain. The Clinical Journal of Pain, 18, 355-365.

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.

van Wijk, R. M., Geurts, J. W., Wynne, H. J., Hammink, E., Buskens, E., Lousberg, R., Knape, J. T., & Groen, G. J. (2005). Radiofrequency denervation of lumbar facet joints in the treatment of chronic low back pain: A randomized, double-blind, sham lesion-controlled trial. Clinical Journal of Pain, 21, 335-344.

Vlaeyen, J. W. S. & Linton, S. J. (2000). Fear-avoidance and its consequences in chronic musculoskeletal pain: A state of the art. Pain, 85, 317-322.

Wieseler-Frank, J., Maier, S. F., & Watkins, L. R. (2005). Immune-to-brain communication dynamically modulates pain: Physiological and pathological consequences. Brain, Behavior, & Immunity, 19, 104-111.

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, 2441-2450.

Weinstein, J. N., Lurie, J. D., Tosteson, T. D., et al. (2008). Surgical vs. nonoperative treatment for lumbar disc herniation: Four-year results for the spine patient outcomes research trial (SPORT). Spine, 33, 2789-2800.

Woolf, C. J. (2011). Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152 (3 Suppl), S2-15.

Yunus, M. B. (2007). The role of central sensitization in symptoms beyond muscle pain, and the evaluation of a patient with widespread pain. Best Practice Research in Clinical Rheumatology, 21, 481-497.

Author: Murray J. McAllister, PsyD

Date of last modification: 4-29-13