What is the Neuromatrix of Pain?

The notion of a neuromatrix of the brain is a theoretical model that explains the nature of pain, including chronic pain. Ronald Melzack, PhD, a psychologist, and one of the founding fathers of the field of pain management as we know it today, developed the theory and published it in a series of papers at the end of the last century.1, 2, 3, 4 Melzack had previously revolutionized the field of pain management in an earlier theory that he had developed and published with his physician colleague, Patrick Wall, in what is known as the gate control theory of pain.5 Few theories in modern science have spawned more empirical research than those of the gate control theory of pain and the neuromatrix of pain. Indeed, while technically theories, the field largely considers these models as accurate explanations of the nature of pain, given the great wealth of empirical evidence that now confirms them. So, what is this notion of the neuromatrix of the brain that explains the nature of pain?

Essentially, the model of the neuromatrix is that the central nervous system, which is made up by the brain and spinal cord, is where pain is produced and that multiple parts of the brain and spinal cord work together in response to stimuli from the body and/or the environment to create the experience of pain. It thus involves two important shifts in our understanding of pain:

  • The brain and spinal cord are what produce pain, not tissue damage
  • Various parts of the central nervous system work together to produce pain

In this way, the location of what produces pain shifts from tissue damage in the body and the peripheral nervous system that surrounds it to the central nervous system.

Neuromatrix model contrasted with the Cartesian model of pain

This model of the neuromatrix stands in contrast to a long held explanatory model of pain that associates the production of pain with tissue damage and its resultant detection by the peripheral nervous system. This latter model tends to equate nociception with pain. Nociception is a term used to refer to nerve impulses, or what are often referred to as "pain signals." In this view, the peripheral nervous system detects painful tissue damage, which then sends "pain signals" to the central nervous system, including the brain, where the pain registers as a conscious experience in the brain. The spinal cord and brain are simply receivers of the pain that is sent from the site of tissue damage by the peripheral nervous system. This explanatory model of pain thus privileges the peripheral nervous system and tissue damage over the brain and spinal cord when it comes to the production of pain. This model was originally developed by the philosopher Rene DesCartes6 and still finds adherents today in certain disciplines within the field of chronic pain management, specifically many interventional pain physicians and spine surgeons, both of whom continue to look for “pain generators” in putative tissue damage (e.g., such as degenerative changes to the spine) and the surrounding peripheral nervous system.

This Cartesian view of pain holds great sway. We hurt ourselves, say, by cutting a finger while chopping vegetables, and the finger hurts. The site of pain is thus easily equated with the cause of pain: what produces the pain is the cut. The peripheral nerves in the finger and hand pick up on the tissue damage and send this information in the form of pain signals to the brain via the spinal cord. The central nervous system, (i.e., the spinal cord and brain), serve the secondary role of receivers of the pain. Their role, as it were, is to register the pain as a conscious experience –- we become conscious of the pain in the finger. What takes primary importance, in this view, is the pain generator of tissue damage and the surrounding peripheral nerves within the area of the tissue damage, in this case, in the finger and hand. This model of pain seems common sense.

Melzack noticed, however, that the Cartesian model of pain doesn’t fit many cases in which we feel pain. He was particularly interested, for instance, in phantom limb pain because the Cartesian model starkly fails to explain its nature (see this brief video on Melzack here). Phantom limb pain is pain in an amputated limb. A person, for example, might feel pain in a foot, even though he no longer has a foot due to, say, a below-the-knee amputation. Phantom limb pain is real pain, but it has no corresponding tissue damage in the area in which the pain is felt. Indeed, there isn’t even any corresponding tissue in the area of pain, for there is no actual limb. As such, the pain generator cannot be in the foot, because the foot is no longer there. Therefore, the central nervous system must be more than a passive receiver of pain signals from the site of injury via the peripheral nervous system. The pain generator, Melzack thus argued, must be in the intact central nervous system.

We don’t have to look to uncommon and intriguing conditions like phantom limb pain to see that the spinal cord and brain must be actively producing pain. A long-known, but little acknowledged, fact about pain is that it tends to have little to no correlation to the extent of tissue damage. This fact stubbornly asserts itself in both research and in the clinic. In studies across multiple pain conditions, objective findings have no clinically significant correlation to pain levels7, 8, 9, 10 (see, for example, this review of the relationship between degenerative disc disease and pain). In clinic, providers see these research findings play out everyday in the wide range of people who present with or without pain. Commonly, people come to clinic with extensive or severe objective findings of some form of tissue damage, which, if the Cartesian model were true, should be exceptionally painful, but these people don’t report pain or report only minimal pain. Just as commonly, still other people present to clinic reporting severe pain without any objective findings of tissue damage or only minimal tissue damage. The Cartesian model of pain would inform us that these latter people shouldn’t have pain or at least not as much pain as they report, but here they are, reporting high levels of pain. The fact that pain has little to no correlation with tissue damage in any of its various forms is one of those stubborn facts that keeps failing to fit the commonly held Cartesian model of pain.

Let’s take some common examples of how this lack of correlation between tissue damage and pain plays out in the clinic and in patients.

Non-specific low back pain is the most common form of low back pain.11, 12 What non-specific means is that the pain in the low back has no specific, identifiable tissue damage that can account for the pain. MRI or CT scans, for instance, can identify no tears in the ligaments or any disc-related degenerative changes to the spine. In other cases, the scans might identify some type of muscular or disc-related abnormalities, but they are of a kind or in a location that would make it impossible to have any direct, causal relationship to the pain that the patient has (such findings are common and called incidental). As such, patients present with real back pain, but have no identifiable tissue damage that might cause it. As indicated, this type of back pain is the most common form of back pain.

All-too-often, what happens in these kinds of cases is that healthcare providers might acknowledge the lack of meaningful correlation between tissue damage and pain, but then look the other way and continue the search for some form of tissue damage, such as degenerative changes in the spine, on which to pursue surgical or interventional procedures. The assumption is that there must be some form of tissue damage, as the Cartesian model dictates, or, if there isn’t, the pain is in some way not as real as it might be were there specific tissue damage. This practice can lead to an exhaustive investigation for the putative “pain generator” in the spine through the use of scans, discographies, diagnostic injections, and various therapies that are pursued on a trial-and-error basis, often leading to multiple interventional pain procedures and/or spine surgeries. This adherence to the Cartesian model of pain fails to heed the stubborn fact that tissue damage tends to have little to no correlation with pain and so must be largely independent of whatever produces pain. It also fails to conform to a wealth of basic pain science that confirms Melzack’s theory that pain lies in the brain, not in putative tissue damage.

Fibromyalgia has long been considered a mysterious condition because it’s a common widespread pain disorder without any identifiable tissue damage despite decades of research attempting to find it. However, it’s only mysterious when we unwittingly hold to the Cartesian model that all real pain is pain attributable to tissue damage that sends "pain signals" via the peripheral nervous system to a passive recipient otherwise known as the central nervous system. If we put down the model and see the reality of those who are presenting to us with fibromyalgia, we make room for the possibility that there must be a different explanation for how humans can come to have pain. We make room for the notion that the central nervous system is what generates pain.

Wittgenstein, who might have rightly laid claim to have been the first non-Cartesian philosopher since DesCartes himself, was fond of observing our human capacity to become captivated by an explanatory model of a particular phenomenon and thus come to see all instances of this phenomenon in the light of the model; in so doing, we subsequently fail to heed, or even see, any of those stubborn instances that fail to fit the model.13 In light of this tendency to become captivated by our explanatory model, he persistently challenged us to look and see those stubborn facts and learn from them – learn to change our perspective to allow for a more encompassing understanding of the phenomenon in question.

This change in our perspective on pain is what Melzack identified and explained in his theory of the neuromatrix of pain. As such, Melzack might rightly lay claim to be the first non-Cartesian pain expert. He looked at pain conditions that don’t fit the Cartesian model, and rather than seeing them as mysterious or not as real in some way as pain that has corresponding tissue damage, he posited an over-arching idea that explains pain of all kinds – pain that has and does not have corresponding tissue damage. In this way, the notion of the neuromatrix of the brain identifies the centrality of pain. It locates the production of pain in the brain, not in tissue damage within the body or its surrounding peripheral nervous system. In so doing, he makes room for understanding how pain is largely independent of tissue damage, something that empirically we keep finding but heretofore did not have a model that allowed for understanding it.

The Product of Multiple Areas of the CNS Working Together

The notion of the neuromatrix also involves the idea that multiple parts of the central nervous system work together to generate pain. The parts of the central nervous system that make up this matrix are the following:

  • Spinal cord
  • Brain stem and thalamus
  • Various parts of the limbic system, such as the hypothalamus, amygdala, hippocampus, anterior cingulate cortex, among others
  • Insular cortex
  • Somatosensory cortex
  • Motor cortex
  • Prefrontal cortex

Each part contributes to various aspects of the experience of pain: the sensory, emotional, cognitive, motoric, behavioral, and conscious aspects. Research over the last thirty years has made significant strides in mapping these various aspects of pain onto corresponding areas of the brain, which work in combination. A full review of this research would be too lengthy to go into here, but a few brief examples would be the consistent findings associating the limbic and insular systems with both the emotional aspects of pain and its intensity,14, 15, 16, 17, the prefrontal cortex with how one makes sense of pain,18, 19, 20 and the somatosensory cortex with where the pain is felt in the body.21, 22, 23

The notion that a matrix of parts within the brain produces pain explains a number of facts about pain, which seem mysterious and inexplicable when holding to the Cartesian model of pain. It has long been known that various factors influence the degree of pain that one has, over and above whatever extent of tissue damage there is. For instance, the degree of attention to pain can influence the level of pain.24, 25, 26 Prior learning about pain, injuries and illness can influence current pain levels.27, 28 The social context in which pain occurs can play a role in whether and how much one has pain.29, 30 The emotional mood state at the time of pain can have a similar role.31, 32 All of these long-known phenomena about pain fail to make sense if we solely equate pain with tissue damage, as in the case of the Cartesian model. However, if we recognize the role of the brain in the production of pain, then all these psychosocial aspects of pain become explainable.

Implications: Changing paradigms of pain; treatment; placebo response

Changing paradigms of pain

The notion of the neuromatrix of pain and the wealth of empirical evidence that confirms it over the last thirty years is inevitably leading to a paradigm shift in how we understand pain. Pain isn’t primarily the result of an orthopedic condition as the Cartesian model has long had us suppose, but rather it is the result of a nervous system condition (or, more specifically, a neuro-endocrine-immune system condition33, 34). Indeed, today, we are witnessing this change in paradigms. Increasingly, experts in pain have come to accept that chronic pain is a condition of the central nervous system, though we still shy away from calling it a brain disorder, perhaps, out of concern for stigmatizing patients. This overall trend, however, will likely continue and one day it may not seem so strange to consider chronic pain a brain disorder or to seek interventions that alter the brain’s neuromatrix when having either acute or chronic pain.

Indeed, even at present, we commonly engage in helping behaviors that beneficially change the neuromatrix of those in acute pain, even though we typically don’t recognize it as such. Take, for example, the common occurrence of a small child who falls down, scrapes her knee, feels pain and subsequently begins to cry; what adults typically do in such situations is to reassure the child (e.g., “You’re okay”), place an adhesive bandage on the scrape, and redirect the child’s attention to some form of play. Such "therapies" typically and readily ameliorate the pain entirely.

In these interactions, we provide reassurance to the child that the harm to her bodily integrity is not dangerous by reassuring her that she is okay. In so doing, we change her belief system about the tissue damage. She had thought that the scrape was dangerous, but upon receiving our reassurance, she now understands that it is something benign. With our reassurance, we don’t downplay or invalidate the pain, but rather take it seriously by attending to it with the adhesive bandage. In this way, we don’t create the possibility in her belief system that we may have missed something in our diagnosis and so perhaps her harm might be dangerous after all. We also don’t create a power struggle over who is right – her and her immediate sense that her tissue damage is dangerous or us in our assurance that it isn’t dangerous. In addition, we use intentional distraction of attention away from the sense of harm that she has. In so doing, we occupy her attention with pleasant experiences, which further reinforce the sense that her harm is really not dangerous. As a result of all these changes in her cognitive, attentional and emotional aspects of pain, her pain ceases. In other words, what we have done in our response to her injury is to change the neuromatrix of her brain. (See, for example, Goodman and McGrath35).

Such changes to the neuromatrices of people are not limited to children. Any patient and clinician can attest to the therapeutic power of a reassurance visit to a healthcare provider. In acute injuries and illnesses of all kinds, a significant amount of therapeutic benefit can occur when we receive a reassuring diagnosis, which we believe because we’ve been taken seriously, and subsequently have become confident that we can go on with our life’s activities. We go from a state, on the one hand, of not knowing the significance and dangerousness of the tissue damage that has occurred and subsequently having become afraid and alarmed, to a state, on the other hand, of certainty in belief that we are safe and can redirect our energies and attention elsewhere. As a result of the upstream cognitive intervention, we come to feel better downstream in our body.

Basic science supports these everyday observations. While a full review of this literature would lead us too far astray, even a cursory look points to how messages to or from the central nervous system regarding harm to bodily integrity can elicit pain.36 or make existing pain worse.37, 38, 39

From this light, we can better appreciate the current trend in the field that encourages a change in the messaging to patients at the time of a consultation for an acute pain episode. The admonition to express a message that ‘hurt doesn’t equal harm’ is a cognitive intervention that changes the neuromatrix of an acute pain condition.

Now, certainly, all ailments don’t necessarily follow this top-down alignment. Pancreatic cancer might be an example that fails to follow a top-down progression. However, decades of research indicate that symptoms mediated by the autonomic nervous system, such as pain, nausea, depression and the like, do.40, 41


For the last forty years or so, the field of chronic pain management has had an established form of treatment that focuses its interventions at the level of the central nervous system in this top-down manner. Moreover, this treatment has about four decades of outcome research showing it to be an effective, if not the most effective, treatment for chronic pain.42, 43, 44, 45, 46, 47, 48, 49 It’s called the interdisciplinary chronic pain rehabilitation program (CPRP). Such programs are an interdisciplinary treatment for chronic pain that involves health psychology, physical therapy, and medication management within a cognitive behavioral and exposure-based milieu. The predominant interventions are cognitive behavioral therapies, mild aerobic exercises both on land and in the pool, use of antiepileptics and antidepressants (either tricyclics or SNRI’s), various forms of relaxation interventions (i.e., diaphragmatic breathing, progressive muscle relaxation, tai chi, mindfulness meditation, yoga), and exposure-based interventions of opioid tapering and maintaining a daily schedule of activities.

The notion of the neuromatrix of the brain explains why and how CPRPs are effective.

The common denominator of all the therapies in a CPRP is that they target the central nervous system, reducing its sensitivity, but also the cognitive, emotional and motoric aspects of pain, among others. They do so by changing how patients make sense of pain, changing their degree of emotional alarm about it, and by reassuringly showing them how to move and engage in activities despite pain. In other words, CPRPs are a top-down intervention: by changing the neuromatrix of the central nervous system one can change the peripheral nervous system and the pain of the associated body parts.

CPRPs commonly fail to make sense to patients, third-party payers, and even some healthcare providers. Patients are often reluctant to pursue it until all therapies that target putative tissue damage have been exhausted. Some healthcare providers fail to refer patients to CPRPs because they continue to recommend therapies targeting putative tissue damage long after it is reasonable to conclude that these therapies aren’t effective. Third-party payers have a long history of readily paying for care that focuses on the putative tissue damage associated with pain and refraining from paying for CPRPs. From the light of our discussion here, we might see why: all these stakeholders tend to understand pain through the Cartesian model that equates pain with tissue damage and so readily seek out, recommend, and pay for bottoms-up therapies, such as interventional pain procedures and surgeries. As we’ve seen, a Cartesian model makes no room for understanding how and why a top-down therapy, such as a cognitive behavioral based CPRP, is effective.

Now that we have the neuromatrix model of pain model and about thirty years of basic pain science to confirm it, we might begin to ask, as a field and as a society, why do we continue to treat so few people with effective treatments that target the central nervous system, such as with CPRPs, and instead treat so many people with less effective treatments that target putative tissue damage, which has little to no correlation with pain?

Placebo response

The neuromatrix model of pain puts what we know about the placebo response in a new light. Perhaps the placebo response is neither mysterious nor to be derided, as it so often is by both clinicians and the public alike. What if, all along, the placebo response has been an unintentional cognitive behavioral intervention that changes the neuromatrix of the brain’s responses and thereby reduces pain? In other words, the placebo response is the result of a complex set of sociocultural beliefs, expectations and conditioning behaviors, which influence the neuromatrix of the brain. As such, it would no longer seem so mysterious and we might no longer snicker when it occurs. From this light, we should respect the placebo response, learn from it, and develop cognitive behavioral interventions that we use intentionally to change the neuromatrix, rather than becoming perplexed when it inadvertently occurs.

The belief that one’s bodily integrity, for instance, is not in danger or is no longer in danger could involve Man on Bed of Nailscorresponding changes in the prefrontal cortex and limbic system, which then produce a cascade of psychophysiological responses, that lead to having no pain or a cessation of pain, respectively. Any number of common social and attentional contexts lead to the aforementioned beliefs and their resultant effects on pain levels: the absence of pain when tissue damage occurs can be brought about, for example, in the passionate excitement of the game for a football player who might otherwise think that he has injured himself; the cessation of an already occurring pain might be due to a ritualized surgical procedure on a patient who has acquired a sociocultural belief system about the nature of his pain and the efficacy of the procedure (see for example, studies by Kirkley, et al.,50 Bradley, et al.,51 Sihvonen, et al.,52 and Moseley, et al.,53 which show the equal effectiveness of various kinds of knee surgeries with placebo, or sham, surgeries). Respectively, in these cases, a belief system keeps pain at bay or reduces it. These long observed phenomena show the power of changing the neuromatrix.

When this phenomenon occurs unintentionally, we tend at present to call it the placebo response. When it happens intentionally within the context of cognitive behavioral therapy or a related CPRP, we call it pain reduction.

Perhaps, we should just call it a change in the neuromatrix of the brain.


The notion of the neuromatrix of the brain is an explanatory model of how pain is produced and therapeutically reduced. Ronald Melzack, PhD, a psychologist, initially developed the model over a series of papers published at the end of the last century. Approximately thirty years of basic science has since confirmed the model and most pain experts now largely consider it an accurate understanding of the nature of pain. The model involves two broad components: 1) pain is produced not by putative tissue damage and the peripheral nervous system that surrounds it, but rather by the central nervous system, i.e., the brain and spinal cord; 2) various parts of the brain and spinal cord work in combination to produce the multiple aspects of the experience of pain. The significance of the neuromatrix model of pain is none other than to change our paradigmatic understanding of the nature of pain. We are presently in the process of letting go of our Cartesian paradigm through which we have understood the nature of pain for the last four centuries. In its place, we are adopting an altogether new yet more helpful paradigm for understanding pain. In so doing, we can now understand how people can have pain whether they have injury or not. We can also now understand why therapies that target the central nervous system, such as cognitive behavioral based CPRPs, have long been shown to be effective. Moreover, we can now better understand why therapies that target putative tissue damage keep failing over the years to be demonstrably effective.54 The model of the neuromatrix of the brain also puts the placebo effect in a new light, as the effect of an inadvertent change in the neuromatrix of the brain.

For more information, please see related topics: central sensitization; the relationship between degenerative disc disease and pain; the changing paradigm in pain management; the mission of the Institute for Chronic Pain to educate the public about empirically-based conceptualizations of pain and its treatments.


1. Melzack, R. & Loeser, J. D. (1978). Phantom body parts in paraplegics: Evidence for a central ‘pattern generating mechanism’ for pain. Pain, 4, 195-210.

2. Melzack, R. (1989). Phantom limbs, the self, and the brain (The D. O. Hebb Memorial Lecture). Canadian Psychologist, 30, 1-16.

3. Melzack, R. (1990). Phantom limbs and the concept of a neuromatrix. Trends in Neurosciences, 13(3), 88-92.

4. Melzack, R. (1999). From the gate to the neuromatrix. Pain, S6, S121-S126.

5. Melzack, R. & Wall, P. D. (1965). Pain mechanisms: A new theory. Science, 150, 971-979.

6. DesCartes, R. (1633/2003). Treatise of Man. Amherst, NY: Prometheus.

7. 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

8. Cheung, K. M., Karppinen, J., Chan, D., Ho, D. W., Song, Y., Sham, P., Cheah, K. S., Leong, J. C., & Luk, K. D. (2009). Prevalence and pattern of lumbar magnetic resonance imaging changes in a population study of one thousand forty-three individualsSpine, 34(9), 934-940.

9. Guermazi, A., Niu, J., Hayashi, D., Roemer, F. W., Englund, M., Neogi, T., Aliabadi, P., McLennan, C. E., & Felson, D. T. (2012). Prevalence of abnormalities in knees detected by MRI based observational study (Framingham Osteoarthritis Study). BMJ, 345, e5339.

10. Register, B., Pennock, A. T., Ho, C. P., Strickland, C. D., Lawand, A., & Philoppon, M. J. (2012). Prevalence of abnormal hip findings in asymptomatic participants. American Journal of Sports Medicine, 40(12), 2720-2724.

11. Balague, F., Mannion, A. F., Pellise, F., & Cedraschi, C. (2012). Non-specific low back pain. Lancet, 379, 482-491.

12. Krismer, M. (2007). Low back pain (non-specific). Best Practice & Research: Clinical Rheumatology, 21(1), 77-91.

13. Wittgenstein, L. (1953). Philosophical Investigations. New York: Macmillan.

14. Rouwette, T., Vanelderen, P., Roubos, E. W., Kozicz, T., & Vissers, K. (2012). The amygdala, a relay station for switching on and off pain. European Journal of Pain, 16(6), 782-792. doi: 10.1002/j.1532-2149.2011.00071.x

15. Price, D. D. (2000). Psychological and neural mechanisms of the affective dimension of pain. Science, 288(5472), 1769-1772.

16. Segerdahl, A. R., Mezue, M., O’Kell, T. W., Farra, J. T. & Tracey, I. (2015). The dorsal posterior insula subserves a fundamental role in human painNature Reviews Neuroscience, 18, 499-500. doi: 10.1038/nn.3969

17. Uddin, L. Q. (2015). Salience processing and insular cortical function and dysfunction. Nature Reviews Neuroscience, 16(1), 55-61. doi: 10.1038/nrn3857

18. Simons, L. E., Elman, I., & Borsook, D. (2014). Psychological processing in chronic pain: A neural systems approachNeuroscience & Biobehavioral Reviews, 39, 61-78. doi: 10.1016/j.neubiorev.2013.12.006

19. Apkerian, A. V., Bushnell, M. C., Treede, R. D., & Zubleta, J. K. (2005). Human brain mechanisms of pain perception and regulation in health and disease. European Journal of Pain. 9(4), 463-484.

20. Atlas, L. Y. & Wager, T. D. (2012). How expectations shape pain. Neuroscience Letters, 520(2), 140-148. Doi: 10.1016/j.neulet.2012.03.039

21. Flor, H. (2012). New developments in the understanding and management of persistent painCurrent Opinion in Psychiatry, 25(2), 109-113. doi: 10.1097/YCO.0b013e3283503510

22. Haggard, P., Iannetti, G. D., & Longo, M. R. (2013). Spatial sensory organization and body representation in pain perception. Current Biology, 23, R164-R176. doi: 10.1016/j.cub.2013.01.047

23. Bushnell. M. C., Duncan, G. H., Hofbauer, R. K., Ha, B., Chen, J.-I., Carrier, B. (1999). Pain perception: Is there a role for primary somatosensory cortex? Proceedings of the National Academy of Sciences, 96(14), 7705-7709.

24. Pincus, T. & Morley, S. (2001). Cognitive-processing bias in chronic pain: A review and integration. Psychological Bulletin: 127(5), 599-617.

25. Bantick, S. J., Wise, R. G., Ploghaus, A., Clare, S., Smith, S. M., & Tracey, I. (2002). Imaging how attention modulates pain in humans using functional MRI. Brain, 125(2), 310-319. doi: 10.1093/brain/awf022

26. Van Damme, S., Legrain, V., Vogt, J., & Crombez, G. (2010). Keeping pain in mind: A motivational account of attention to pain. Neuroscience & Biobehavioral Reviews, 34, 204-213. doi: 10.1016/j.neubiorev.2009.01.005

27. Wiech, K., Vandekerckhove, J., Zaman, J., Tuerlinckx, F., Vlaeyan, J. W., & Tracey, I. (2014). Influence of prior information on pain involves biased perceptual decision-making. Current Biology, 24(15), R679-R681. doi: 10.1016/j.cub.2014.06.022

28. Goubert, L., Vlaeyan, J. W., Crombez, G., & Craig, K. D. (2011). Learning about pain from others: An observational learning account. Journal of Pain, 12(2), 167-174. doi: 10.1016/j.pain.2010.10.001

29. Eisenberger, N. I., Master, S. L., Inagaki, T. K., Taylor, S. E., & Shirinyan, D. (2011). Attachment figures activate a safety signal-related neural region and reduce pain experience. Proceedings of the National Academy of Science, 108(28), 11721-11726. doi: 10.1073/pnas.1108239108

30. Montoya, P., Larbig, W., Braun, C., Preissl, H., & Birbaumer, N. (2004). Influence of social support and emotional context on pain processing and magnetic brain responses in fibromyalgia. Arthritis & Rheumatism, 50(12), 4035-4044. doi: 10.1002/art.20660

31. Wiech, K. & Tracey, I. (2009). The influence of negative emotions on pain: Behavioral effects and neural mechanisms. NeuroImage, 47, 987-994. doi: 10.1016/j.neuroimage.2009.05.059

32. Villemure, C. & Bushnell, M. C. (2009). Mood influences supraspinal pain processing separately from attention. Journal of Neuroscience, 29(3), 705-715. doi: 10.1523/jneurosci.3822-o8.2009

33. Melzack, R. (1999). Pain and stress: A new perspective. In Gatchel, R. J. and Turk, D. C. (Eds.), Psychosocial factors in pain (pp. 89-106). New York: Guilford Press.

34. 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(2), 122-145. doi: 10.1016/j.jpain.2007.09.006

35. Goodman, J. E. & McGrath, P. J. (2003). Mother's modeling influences children's pain during a cold pressor task. Pain, 104(3), 559-565.

36. Harvie, D. S., Broecker, M., Smith, R. T., Meulders, A., Madden, V. J., & Moseley, G. L. (2015). Bogus visual feedback alters onset of movement-evoked pain in people with neck pain. Psychological Science, 26(4), 385-392. doi: 10.1177/0956797614563339

37. Moseley, G. L. & Arntz, A. (2007). The context of a noxious stimulus affects the pain it invokes. Pain, 133(1-3), 64-71.

38. Arntz, A. & Claassens, L. (2004). The meaning of pain influences its experienced intensity. Pain, 109(1-2), 20-25.

39. Moseley, G. L., Zalucki, N., Birklein, F., Marinus, J., van Hilten, J. J., & Luomajoki, H. (2008). Thinking about movement hurts: The effect on motor imagery on pain and swelling in people with chronic arm painArthritis Care & Research, 59(5), 623-631. doi: 10.1002/art.23580

40. Papakostas, Y. G. & Daras, M. D. (2001). Placebos, placebo effect, and the response to the healing situation: The evolution of a concept. Epilepsia, 42, 1614-1625.

41. Wampold, B. E., Minami, T., Tierney, S. C., Baskin, T. W., & Bhati, K. S. (2005). The placebo is powerful: Estimating placebo effects in medicine and psychotherapy from randomized clinical trials. Journal of Clinical Psychology, 61(7), 835-854. doi: 10.1002/jclp.20129

42. Flor, H., Fydrich, T. & Turk, D. C. (1992). Efficacy of multidisciplinary pain treatment centers: A meta-analytic review. Pain, 49, 221-230.

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

44. 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.

45. Busch, H., Bodin, L., Bergstrom, G., & Jensen, I. B. (2011). Patterns of sickness absence a decade after pain-related multidisciplinary rehabilitation. Pain, 152, 1727-1733.

46. Patrick, L. E., Altmaier, E. M., & Found, E. M. (2004). Long-term outcomes in multidisciplinary treatment of chronic low back pain: Results of a 13-year follow-up. Spine, 29(8), 850-855.

47. Hauser, W., Bernardy, K., Arnold, B., Offenbacher, M., & Schiltenwolf, M. (2009). Efficacy of multicomponent treatment in fibromyalgia syndrome: A meta-analysis of randomized controlled trials. Arthritis & Rheumatology, 61(2), 216-224. doi: 10.1002/art.24276

48. Guzman, J., Esmail, R., Karjalainen, K., Malmivaara, A., Irvin, E., & Bombardier, C. (2005). Multidisciplinary rehabilitation for chronic low back pain: Systematic review. BMJ, 322(7301), 1511-1516.

49. Gatchel, R. J., McGeary, D. D., McGeary, C. A., & Lippe, B. (2014). Interdisciplinary chronic pain management: Past, present, and future. Amercian Psychologist, 69(2), 119-130. doi: 10.1037/a0035514

50. Kirkley, A., Birmingham, T. B., Litchfield, R. B., Griffin, J. R., Willits, K. R... Fowler, P. J. (2008). A randomized trial of arthroscopic knee surgery for osteoarthritis of the kneeNew England Journal of Medicine, 359(11), 1097-1107. doi: 10.1056/NEJMoa0708333

51. Bradley, J. D., Heilman, D. K., Katz, B. P., G'Sell, P., Wallick, J. E., & Brandt, K. D. (2002). Tidal irrigation as treatment for knee osteoarthritis: A sham-controlled, randomized, double-blinded evaluation. Arthritis & Rheumatism, 46(1), 100-108.

52. Sihvonen, R., Paavola, M., Malmivaara, A., Itala, A., Joukainen, A., Nurmi, H., Kalske, J., & Jarvinen, T. L. (2013). Arthroscopic partial meniscectomy vs. sham surgery for a degeneratiev meniscal tearNew England Journal of Medicine, 369(26), 2515-2524. doi: 10.1056/NEJMoa1305189

53. Moseley, J. B., O'Malley K., Petersen, N. J., Menke, T. J., Brody, B. A., Kuykendall, D. H., Hollingsworth, J. C., Ashton, C. M., & Wray, N. P. (2002). A controlled trial of arthroscopic knee surgery for osteoarthritis of the kneeNew England Journal of Medicine, 347(2), 81-88. doi: 10.1056/NEJMoa013259

54. Deyo, R. A., Mirza, S. K., Turner, J. A., & Martin, B. I. (2009). Overtreating back pain: Time to back off? Journal of the American Board of Family Medicine, 22(1), 62-68. doi: 10.3122/jabfm.2009.01.080102

Date of publication: May 23, 2015

Date of last modification: May 12, 2017

Murray J. McAllister, PsyD, is a pain psychologist and consults to health systems on improving pain. He is the editor and founder of the Institute for Chronic Pain (ICP). The ICP is an educational and public policy think tank. In its mission is to lead the field in making pain management more empirically supported, the ICP provides academic quality information on chronic pain that is approachable to patients and their families. 

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