An Evolving Understanding of Chronic Pain: Challenges and Opportunities

A Brief History

Dr. Vining

Not so long ago, our understanding of pain was less complicated. Apart from pain associated with psychological disorders, there was essentially one type, presumed to be caused by injury, dysfunction or irritation of a body part. Pain duration was classified into three categories: acute, subacute, and chronic. But the pain model was incomplete, unable to explain common situations.

There were no plausible explanations for how or why some people with obvious injury or dysfunction experienced little or no pain. Conversely, there was no explanation, other than malingering, for why some people had pain without any evidence of injury or anatomical problem. Why some people with advanced joint degeneration could remain active with little or no pain while others could not, was also a mystery.

In 1965, in what is credited as a turning point in pain science, Melzak and Wall published a paper that helped move research toward a new model.(1) The gate theory proposed pain was the product of multiple adaptive nervous system mechanisms.(2) Subsequent research helped confirm that pain is not produced in body tissues. Instead, it is a perception created in the brain from a combination of sensory and/or central nervous system activity. These changes represented a fundamental shift in the way we interpret pain. With this new knowledge, pain was not dependent on whether tissues were injured or inflamed, rather a net result of cognitive, limbic and sensory activity.

More recent research has built on this new model, describing how factors such as sleep loss and social disconnection can contribute to pain sensitivity (3–5). Research also led to a better understanding of how the nervous system maladapts to chronic pain, through processes collectively referred to as central sensitization. It is now very clear that the nervous system has the capacity to adapt in ways that tend to amplify pain.(6)

Practical Challenges

Clinical evaluation can be challenging considering current pain science concepts. For example, a common practice is to ask patients about activities that aggravate symptoms. Presumably, a painful movement (twisting, bending, or extending) irritates an injured or dysfunctional tissue, causing pain. Palpatory tenderness suggests inflamed, dysfunctional or injured tissue lies beneath the palpated area. However, those presumptions are based on an outdated and oversimplified pain model, one that makes presumptions that may not be accurate.

Recall that pain can occur without tissue damage and pain severity can be exaggerated with central sensitization mechanisms. Accurately interpreting a painful activity requires synthesizing a diverse array of information, such as the length of time pain has existed, the setting when the pain began (e.g., high stress, traumatic event), a patient’s concerns about what the pain represents (e.g., a minimal annoyance, possible life-changing problem), and other relevant comorbid, psychosocial, and environmental factors. Because pain perception is influenced by so many different factors, pain can occur during activities that can be therapeutic. This seeming paradox can be challenging for patients to understand and clinicians to explain.

Fortunately, there are resources to help clinicians address these challenges. For example, Blickenstaff et al., offer examples of helping patients understand differences between harmful and non-harmful activities, to help patients engage in therapeutic activities that are physically uncomfortable.(7) Another resource is authored by Louw and colleagues, who provide examples of how to use simple metaphors and other strategies to teach people about pain.(8) Both articles offer examples of how to practically apply current pain science principles in practice.


Perhaps because the science of pain is constantly evolving, some misconceptions about chronic pain have emerged.

Misconception #1: Chronic pain is pain lasting over 12-weeks.
This misconception oversimplifies chronic pain as defined only by time. Perhaps the best examples of chronic spine-related pain are published in a series of articles by Kongstead and colleagues. (9–11) Some people experience relatively constant pain over long periods. For others, pain waxes and wanes without ever fully resolving. Some people experience pain in brief episodes, separated by asymptomatic periods. However, a new episode of a longstanding problem is often a re-emergence of chronic pain, rather than a separate acute condition.

Misconception #2: Central sensitization and chronic pain are synonymous.
The relationship between central sensitization and chronic pain is not direct. Pain must be present for a relatively long period for the nervous system to adapt. Therefore, central sensitization is dependent on chronic pain. But it is wrong to presume all people with chronic pain have central sensitization. Many factors influence when, or if, someone develops central sensitization. As an example, Taylor and Kerry artfully describe an example of a patient who experienced pain for 35 years without developing central sensitization.(12)

Misconception #3: Central sensitization and nociplastic pain are synonymous.
Central sensitization describes a set of nervous system adaptations causing increased pain sensitivity. Recently, the term “Nociplastic pain” was introduced, describing  the pain caused by the collective effects of nervous system sensitization.(13) Before the term nociplastic pain was introduced, there was no standard terminology. Now, terms such as “chronic pain syndrome” and “central pain” are obsolete.

Misconception #4: Nociplastic pain means all symptoms are nervous system generated and there is no physical component.
The presence of nociplastic pain means that some symptom components are augmented by nervous system sensitization. People with nociplastic pain can also have a physical component. One great challenge for clinicians is in identifying if nociplastic pain plays a major, minor or non-contributory role in symptoms.

Currently, there is no method of identifying nociplastic pain with 100% certainty. However, the International Association for the Study of Pain has developed diagnostic criteria that can help. Meeting each of the four criteria below suggests likely nociplastic pain.(13)

  1. Pain of at least three months duration.
  2. Regional rather than discrete pain distribution.
  3. Pain that cannot entirely be explained by nociceptive or neuropathic mechanisms.
  4. Clinical signs of pain hypersensitivity (i.e., mechanical, heat or cold allodynia, and/or painful after-sensations) that are at least present in the region of pain.

Pain science has provided a far more complex understanding of pain, especially chronic pain. This complexity presents many challenges. It also presents new opportunities to help patients learn, to recognize and address potential factors influencing symptoms, and to offer more informed and targeted treatment and self-management advice.

Dr. Vining is associate dean of clinical research, as well as a professor, at the Palmer Center for Chiropractic Research, Palmer College of Chiropractic, in Davenport, Iowa.

  1. Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965 Nov 19;150(3699):971–9.
  2. Mendell LM. Constructing and Deconstructing the Gate Theory of Pain. Pain. 2014 Feb;155(2):210–6.
  3. Krause AJ, Prather AA, Wager TD, Lindquist MA, Walker MP. The Pain of Sleep Loss: A Brain Characterization in Humans. J Neurosci Off J Soc Neurosci. 2019 Mar 20;39(12):2291–300.
  4. Bendapudi NM, Berry LL, Frey K a, Parish JT, Rayburn WL, Bialosky JE, et al. The neural bases of social pain: Evidence for shared representations with physical pain. Pain. 2013;47(7):301–4.
  5. Eisenberger NI. The pain of social disconnection: examining the shared neural underpinnings of physical and social pain. Nat Rev Neurosci. 2012 May 3;13(6):421–34.
  6. Woolf CJ. Central sensitization: Implications for the diagnosis and treatment of pain: Pain. 2011 Mar;152(Supplement):S2–15.
  7. Blickenstaff C, Pearson N. Reconciling movement and exercise with pain neuroscience education: A case for consistent education. Physiother Theory Pract. 2016 Jul;32(5):396–407.
  8. Louw A, Zimney K, O’Hotto C, Hilton S. The clinical application of teaching people about pain. Physiother Theory Pract. 2016;32(5):385–95.
  9. Kongsted A, Kent P, Axen I, Downie AS, Dunn KM. What have we learned from ten years of trajectory research in low back pain? BMC Musculoskelet Disord. 2016 May 21;17:220.
  10. Kongsted A, Kent P, Hestbaek L, Vach W. Patients with low back pain had distinct clinical course patterns that were typically neither complete recovery nor constant pain. A latent class analysis of longitudinal data. Spine J Off J North Am Spine Soc. 2015 May 1;15(5):885–94.
  11. Kongsted A, Hestbæk L, Kent P. How can latent trajectories of back pain be translated into defined subgroups? BMC Musculoskelet Disord. 2017 Jul 3;18(1):285.
  12. Taylor AJ, Kerry R. When Chronic Pain Is Not “Chronic Pain”: Lessons From 3 Decades of Pain. J Orthop Sports Phys Ther. 2017;47(8):515–7.
  13. Nijs J, Lahousse A, Kapreli E, Bilika P, Saraçoğlu İ, Malfliet A, et al. Nociplastic Pain Criteria or Recognition of Central Sensitization? Pain Phenotyping in the Past, Present and Future. J Clin Med. 2021 Jul 21;10(15):3203.