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.

These 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: April 29, 2013

Murray McAllister

Murray J. McAllister, PsyD, is a pain psychologist, and the founder and editor of the Institute for Chronic Pain. He holds a Doctor of Psychology degree from Antioch University, New England, and a Master's degree in philosophy from the University of Oregon. He also consults to pain clinics and health systems on redesigning pain care delivery to make it more empirically supported and cost effective. Dr. McAllister is a frequent presenter to conferences and is a published author in peer reviewed journals. His current research interests are in the relationships between fear-avoidance, pain catastrophizing, and perceived disability.

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