“Pain is inevitable. Suffering is optional.” ― Haruki Murakami
Types of pain.
Although it’s also covered in our Pain 101: Acute Pain article, if you’ve jumped straight to this piece, it’s best to do a quick rehash of how pain is defined and classified.
Pain is defined as: “An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage [1].”
Pain can be classified by its duration:
Acute pain: 0-6 weeks
Subacute pain: 6-12 weeks
Chronic pain: 12 weeks and beyond
Pain can also be classified by its mechanism [2]:
Nociceptive pain arises from actual or threatened damage to organs, skin, joints, and muscle tissues.
Neuropathic pain originates in the nerves themselves, rather than in damaged organs or tissues.
Neuroplastic pain: pain that occurs WITHOUT damage to the nerves or other tissue.
In this article, we will discuss chronic/neuroplastic pain. Though categorized differently, we can use the terms interchangeably for the sake of simplicity. As we’ll cover, chronic pain is almost always neuroplastic, and neuroplastic pain is likely always chronic.
Chronic pain by the numbers.
Chronic pain is one of the largest, medically unsolved problems facing society. It is the number one cause of disability worldwide. Pain-related problems account for up to 80% of visits to physicians. The prevalence of chronic pain can range from 10.1% to 55.2% of the populations studied [3]. This affects over 100 million adults in the U.S. and costs about 560 to 645 billion dollars in both out-of-pocket cost and cost of lost productivity [4].
When does acute pain become chronic?
In normal circumstances, after an injury occurs, the body heals and pain decreases to a point where it is no longer perceived.
“It is generally held that when pain persists beyond the expected time frame for resolution and recovery from tissue injury, this constitutes the bridge from acute to chronic pain [5]”.
There is a consensus among the scientific literature that any pain beyond 3 months, regardless of the severity of the injury, is chronic pain. Unfortunately, about 20% of acute pain episodes become chronic [6].
Why does acute pain become chronic?
1. The primary driver of chronic pain is persistent pain.
Nociceptors are the receptors at the end of nerves that sense pain. They are found in the skin, muscles, joints, and internal organs. The ongoing activation of these receptors, and the subsequent firing of the associated nerves, causes the nerves to become sensitized. Sensitization in medical context means to be abnormally or excessively susceptible to something (in this case, more susceptible to a stimulus that may lead to the experience of pain).
This happens first in the periphery, in the nerves outside of the brain and spinal cord. The same process next occurs in the nerves of the brain and spinal cord, also called the central neurons. This peripheral sensitization, and later central sensitization, leads towards the chronic pain state.
Central sensitization has gained a great deal of attention in the scientific literature and has become synonymous with chronic pain. It has been defined in many ways but there is a consensus that hyperexcitability of the nerves is the core mechanism of central sensitization [7].
“The outcome of the processes involved in central sensitization is an increased responsiveness to a variety of peripheral stimuli including mechanical pressure, chemical substances, light, sound, cold, heat, and electrical stimuli [8].” This is a hugely important aspect of sensitization.
You are not only more sensitive to things that would normally cause pain, but also to sensations that normally would not.
Inflammation that occurs after an injury plays a role in the sensitization process. This is covered more in another post.
2. Another factor that may predispose a person to chronic pain is the nature of the injury itself. For example, low back pain becomes chronic in about 20% of cases [9]. Non-whiplash neck pain becomes chronic in about 10% of cases, but whiplash-related neck pain is up to 40% of cases [10]. Migraine headaches become chronic about 3% of the time [11]. Some diseases are synonymous with central sensitization, including fibromyalgia, chronic fatigue syndrome, and irritable bowel syndrome.
3. Finally, it’s important to mention that psychological and social factors play a role in pain becoming chronic. Evidence indicates that anxiety, depression, fear avoidance, and pain catastrophizing potentially lead to the development of chronic pain [12].
How is chronic pain different?
Acute pain, although perceived differently from individual to individual, is correlated at least somewhat with damaged structures. Think of acute pain as a hardware problem on a computer. Let’s say you dropped your keyboard and the spacebar broke. The solution is quite simple, fix the spacebar. Lucky for us, the body is a self-healing organism, and can fix its own spacebar (at times, it may need some outside help).
Chronic pain is often not correlated with damaged structures, but maladaptive changes to the body’s nervous system. Chronic pain is a software problem. It’s like your keyboard not working because there is a malfunctioning keyboard driver (the software component that lets your keyboard communicate with your computer). The key to this fix, is downloading a new driver, which corrects the input. We’ll cover this more in other articles.
Is chronic pain observable?
Yes, but not really. Brain imaging studies have consistently revealed changes in brain function and anatomy in patients with chronic pain [13]. This change in neural architecture and function is where we get the term ‘neuroplastic’ pain.
However, these studies are not routinely prescribed to 'observe' a patient's pain. They are more often used in presurgical planning, fundamental cognitive neuroscience investigations, and behavior modification and training [14].
It’s not just “In your head.”
It is vitally important to understand that chronic pain is real, it is not imagined, and it is not just “in your head.” Though it may not be completely understood, there are specific mechanisms that lead to the process of our experience of chronic pain. You and I don’t need to know these exact mechanisms. It's important for researchers, drug makers, etc… But I’m assuming if you’re reading this, you’re neither.
If a doctor has told you the pain is “in your head,” he or she is technically correct. Pain is experienced via the interpretation of electrical impulses by the brain, which is located in your head. But such a statement implies that the pain is “made up” or not “real.”
The technical term for “made up” pain is psychogenic pain. The main mechanism proposed for the development of this condition is psychological trauma and suppression of painful emotions, which often happen in childhood but can happen later in life as well [15-16].
The amount of research done on psychogenic pain is sparse [17]. It is undoubtedly real. Studies investigating hypnosis and nocebo effects demonstrate this. Efforts have been taken to estimate the prevalence of psychogenic pain, which has proven difficult to measure. Estimates are as low as 1% and as high as 10% of cases. The main difference between chronic pain and psychogenic pain is chronic pain can be medically explained, and psychogenic pain cannot.
The future of chronic pain.
The first step to solving a problem is knowing you have one. Chronic pain is now beginning to be recognized as a disease in and of itself. The World Health Organization (WHO) in association with the International Association for the Study of Pain (IASP) is implementing diagnostic codes for chronic pain that will be placed in the International Classification of Diseases Version 11 (ICD-11). Chronic/neuroplastic pain would be treated as its own disease.
This may seem like a small thing but I believe it’s a significant advancement in the treatment of chronic pain. Correctly recognizing and diagnosing pain as the primary riddle to solve, helps guide patients towards more appropriate and effective care. This of course would save money and time via a reduction in unnecessary medical studies. More importantly, it would reduce the suffering that so many in chronic pain experience.
Lastly, it’s worth noting that pain as a scientific study is relatively new. There’s a lot we still don’t know. Notwithstanding, a couple of positive advancements have been made.
The biopsychosocial model of treating pain takes into account the biological, psychological, and social aspects of the person being treated. This is a major improvement over the previous biomedical model when it was assumed that pain was in a 1:1 ratio with tissue injury.
Recognizing that pain is more than just a signal equal in magnitude to damage, multimodal pain management systems have begun to emerge, which include drug, non-drug, and self-management interventions.
Summary, Key Points:
Chronic pain is prevalent within the population.
There are physiological mechanisms that lead to the progression of chronic pain.
Some injuries are more likely to become chronic than others.
Psychological factors are involved.
It’s observable, but not routinely tested.
Chronic pain is real; it’s not just in your head.
The science of pain is advancing; improvements in treatment are being made.
Additonal Resources
Check out this free, pain resources book by Dr. Greg Lehman BKin, MSc, DC, MScPT here: http://www.greglehman.ca/pain-science-workbooks
A free pdf/book on “Understanding Persistent Pain” put out by the Tasmanian Health Service:
Lots of tools and resources here: https://www.paintoolkit.org/
Additional resources here: https://painsciencecenter.com/how-to-utilize-the-filing-cabinet/
Glossary
Sensory: of or relating to your physical sense. A physical feeling: something that your body experiences.
Receptors: A nerve ending that senses changes in light, temperature, pressure, etc., and causes the body to react in a particular way.
Periphery: The part of a body away from the center; the outer part or surface.
Stimuli: Something that causes something else to happen, develop, or become more active.
Fear avoidance: refers to the avoidance of movements or activities based on the fear of increased pain or re-injury [18].
Pain catastrophizing: as an exaggerated negative orientation toward actual or anticipated pain experiences [19].
Maladaptive: Unsuitable or counterproductive.
Input: what is put in, taken in, or operated on by any process or system.
Plastic: Able to change and adapt, especially by acquiring alternative pathways for sensory perception or motor skills. Used of the central nervous system.
Nocebo: A substance that causes undesirable side effects as a result of a patient's perception that it is harmful rather than as a result of a causative ingredient.
Multimodal: Using or relying on multiple methods, e.g., to treat an illness.
Works Cited
1. 1. “IASP Announces Revised Definition of Pain.” International Association for the Study of Pain (IASP), 16 July 2020, www.iasp-pain.org/publications/iasp-news/iasp-announces-revised-definition-of-pain/.
2. Hush, Julia M, et al. “Untangling Nociceptive, Neuropathic and Neuroplastic Mechanisms Underlying the Biological Domain of Back Pain.” Pain Management, vol. 3, no. 3, May 2013, pp. 223–236, 10.2217/pmt.13.11. Accessed 8 Nov. 2021.
3. Voscopoulos, C, and M Lema. “When Does Acute Pain Become Chronic?” British Journal of Anaesthesia, vol. 105, Dec. 2010, pp. i69–i85, 10.1093/bja/aeq323. Accessed 4 Jan. 2022.
4. Hruschak, Valerie, and Gerald Cochran. “Psychosocial Predictors in the Transition from Acute to Chronic Pain: A Systematic Review.” Psychology, Health & Medicine, vol. 23, no. 10, 28 Feb. 2018, pp. 1151–1167, 10.1080/13548506.2018.1446097. Accessed 15 Feb. 2022.
5. McGreevy, Kai, et al. “Preventing Chronic Pain Following Acute Pain: Risk Factors, Preventive Strategies, and Their Efficacy.” European Journal of Pain Supplements, vol. 5, no. 2, 1 Nov. 2011, pp. 365–376, www.sciencedirect.com/science/article/abs/pii/S1754320711000149, 10.1016/j.eujps.2011.08.013. Accessed 27 Apr. 2020.
6. Dahlhamer, James, et al. “Prevalence of Chronic Pain and High-Impact Chronic Pain among Adults — United States, 2016.” MMWR. Morbidity and Mortality Weekly Report, vol. 67, no. 36, 14 Sept. 2018, pp. 1001–1006, www.cdc.gov/mmwr/volumes/67/wr/mm6736a2.htm?s_cid=mm6736a2_w, 10.15585/mmwr.mm6736a2.
7. den Boer, Carine, et al. “Central Sensitization in Chronic Pain and Medically Unexplained Symptom Research: A Systematic Review of Definitions, Operationalizations and Measurement Instruments.” Journal of Psychosomatic Research, vol. 117, Feb. 2019, pp. 32–40, 10.1016/j.jpsychores.2018.12.010. Accessed 4 Jan. 2022.
8. 20. Nijs, Jo, et al. “Recognition of Central Sensitization in Patients with Musculoskeletal Pain: Application of Pain Neurophysiology in Manual Therapy Practice.” Manual Therapy, vol. 15, no. 2, Apr. 2010, pp. 135–141, 10.1016/j.math.2009.12.001. Accessed 4 Jan. 2022.
9. National Institute of Neurological Disorders and Stroke. “Low Back Pain Fact Sheet | National Institute of Neurological Disorders and Stroke.” Nih.gov, 2000, www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Low-Back-Pain-Fact-Sheet.
10. Binder, Allan. Neck Pain. © BMJ Publishing Group Ltd 2008., 2007.
11. “Chronic Migraine | American Migraine Foundation.” American Migraine Foundation, 2018, americanmigrainefoundation.org/resource-library/chronic-migraine/.
12. Hruschak, Valerie, and Gerald Cochran. “Psychosocial Predictors in the Transition from Acute to Chronic Pain: A Systematic Review.” Psychology, Health & Medicine, vol. 23, no. 10, 28 Feb. 2018, pp. 1151–1167, 10.1080/13548506.2018.1446097. Accessed 17 Dec. 2021.
13. Price, Theodore J., et al. “Transition to Chronic Pain: Opportunities for Novel Therapeutics.” Nature Reviews Neuroscience, vol. 19, no. 7, 15 May 2018, pp. 383–384, 10.1038/s41583-018-0012-5. Accessed 4 Jan. 2022.
14. Glover, Gary H. “Overview of Functional Magnetic Resonance Imaging.” Neurosurgery Clinics of North America, vol. 22, no. 2, Apr. 2011, pp. 133–139, 10.1016/j.nec.2010.11.001. Accessed 11 Jan. 2022.
15. Pain Medicine PRESIDENT’S MESSAGE Psychogenic Pain-What It Means, Why It Does Not Exist, and How to Diagnose It.
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(https://www.sciencedirect.com/science/article/pii/S187638201000199X)
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18. “Fear-Avoidance Model - an Overview | ScienceDirect Topics.” Www.sciencedirect.com, www.sciencedirect.com/topics/medicine-and-dentistry/fear-avoidance-model.
19. “Pain Catastrophizing - an Overview | ScienceDirect Topics.” Sciencedirect.com, 2015, www.sciencedirect.com/topics/medicine-and-dentistry/pain-catastrophizing. Accessed 13 Jan. 2020.
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