Chronic Pain

Chronic Pain Explained[edit | edit source]

Back pain image.jpg

Chronic pain is on the rise with an estimated 10-20% of the population reporting chronic or recurrent pain.[1] Chronic pain is a leading source of human suffering and disability. [2] The factors that predict the development of chronic pain following an acute episode of pain do not relate to any 'biological' factors such as findings on physical examination, or change on X-ray, but to what are termed 'psychosocial variables', such as mood, stress and the social situation in which the pain occurs.

When pain persists in spite of medical treatment, as is the case in chronic pain syndromes, the issues become even more complex. 

  • The patient finds themselves in a vicious cycle of pain, which is not solely due to the progression of the disease (the pathology in the tissues).
  • A person who has pain, especially on movement, tends to avoid doing things that provoke their symptoms.
  • The person may rest, but unfortunately, this is not beneficial as it leads to secondary stiffness and weakness, worsening the symptoms that the individual is trying to avoid.

Inability to function leads to a loss of role and self-esteem. Other issues then arise, which may include financial hardship and strained relationships, side effects from medications and lack of sleep.1 The Global Burden of Disease Study 2013 evaluated “years lived with disability” (YLDs: the prevalence multiplied by a disability-weighting factor) for a broad range of diseases and injuries in 188 countries. The single greatest cause of YLDs around the world was chronic low back pain, followed by major depressive disorder. Other frequent causes of YLDs include chronic neck pain, migraine, osteoarthritis, other musculoskeletal disorders, and medication overuse headache.[3] These various difficulties cause worry and low mood. Treatments may be attempted through desperation rather than effectiveness with a high risk of failure. This leads to further worsening of mood which fuels a sense of desperation.

The Difference Between Acute and Chronic Pain[edit | edit source]

Previously pain was described using the biomedical model with a reductionist view (i.e. pain was derived from a specific physical pathology). Social, psychological and behavioral mechanisms were dismissed as irrelevant and of no importance to understanding pain.[4] This is a grossly oversimplified model and now we understand that pain is more than a response to a physical stimulus. Thus, in recent years several models of pain models have been created to explain and develop our understanding of pain. 

Acute pain can be defined as:

the normal, predicted physiological response to an adverse chemical, thermal or mechanical stimulus… associated with surgery, trauma and acute illness.[5]

As the definition states, acute pain is a predicted response to a stimulus. If you have had surgery to repair a fractured hip, there will be a usual pattern of pain and rate of recovery based upon the patient's demographics. However, to take this definition further one could say that pain is:

a complex perceptual phenomenon that involves a number of dimensions including (but not limited to) intensity, quality, time, course and personal meaning.[6] 

This definition incorporates the modern thinking of pain, not just acute pain but pain as a whole. The first definition is still true in the fact that acute pain is predictable and does follow a pattern but the second quote reflects the more complex nature of pain and is a reminder that pain should not be thought of as the same for all patients. It becomes even more complex when pain changes from the predictable pattern of duration and nature to an unpredictable and unexplained phenomenon that exceeds the usual duration of healing and becomes chronic.

Chronic pain can be defined as when:

pain persists for 3 months or longer, it is considered chronic[7] and, while not necessarily maladaptive[8][9], often leads to physical decline, limited functional ability and emotional distress. Chronic primary pain is defined as pain in one or more anatomical regions that persists or recurs for longer than 3 months and is associated with significant emotional distress or functional disability (interference with activities of daily life and participation in social roles) and that cannot be better accounted for by another chronic pain condition. This is a new definition, which applies to chronic pain syndromes that are best conceived as health conditions in their own right.[10]Chronic secondary pain syndromes are linked to other diseases as the underlying.

Although this quote only gives the time duration there are many others which consider chronic pain to be unexplained, irregular, unique and incredibly dependent upon the individuals' personal beliefs and coping strategies and it is this chronic pain which is subject to a large amount of study and psychological management strategies. This is in part due to the impact it has on healthcare systems worldwide common chronic pain problems cost eg. U.S.A - US$60 billion per year[4]; UK - somewhere in the region of £5 billion per year[11]. There are millions of lost workdays throughout the world subsequently it is a crucial area in which treatment and management are continually being developed.

Key Models to Understand Pain[edit | edit source]

Pain Gate Theory[edit | edit source]

The pain gate theory (PGT) was first proposed in 1965 by Melzack and Wall[12], and is a commonly used explanation of pain transmission, it was one of the first models to incorporate biological and psychological mechanisms within the same model.[4] Thinking of pain theory in this way is very simplified and may not be suitable in some contexts, however, when discussing pain with patients this description can be very useful.

In order to understand the PGT, the sensory nerves need to be explained. At its most simple explanation, there are 3 types of sensory nerves involved in the transmission of noxious stimuli[13].

  1. A-β fibres - Large diameter and myelinated - Touch, pressure, vibration - Faster
  2. A-δ fibres - Small diameter and myelinated - Pain (mechanical, thermal) - Fast
  3. C fibres - Small diameter and un-myelinated - Pain (throbbing or burning) - Slow

The size of the fibres is an important consideration as the bigger a nerve is the quicker the conduction, additionally conduction speed is also increased by the presence of a myelin sheath, subsequently large myelinated nerves are very efficient at conduction. This means that A-β fibres are the quickest of the 3 types followed by A fibres and finally C fibres[14].

The interplay between these nerves is important but it is not the whole story, as you can see only two of these nerves are pain receptors.  A-β fibres are sensory in terms of touch, pressure and vibration, but it has been suggested that these fibres conduct fast nociceptive signals.[15] The A-δ fibres and C fibres are traditionally considered as the pain-conducting fibres.[16] All of these nerves synapse onto projection cells which travel up the spinothalamic tract of the CNS to the brain where they go via the thalamus to the somatosensory cortex, the limbic system and other areas[17].

The gate theory for pain relates to the concept proposed by Melzack and Wall in 1965 that both first-order mechanical afferents and first-order nociceptive afferents synapse onto the same second-order neurons.[12] The hypothesis, then, is that the predominant first-order activity would determine the activity of the second-order neuron. If the mechanoreceptive information is more active, then that information is transmitted, effectively blocking or closing the gate on the nociceptive information at the level of the dorsal horn. When the smaller, slower fibres are stimulated the inhibitory interneurons do not act, so the gate is 'open' and pain is sensed.[12] When the larger A-β fibres are stimulated they reach the inhibitory interneurons faster and, as larger fibres inhibit the interneuron from working, and the gate is 'closed'. This is why after you have stubbed your toe, or bumped your head, rubbing it helps as you are stimulating the A-β fibres which close the gate[12]

In addition to the idea of the different nerve types influencing whether or not the gate is open or not, mood and cognition also influence the status of the gate in a "Top Down" fashion influencing the perception of the pain further[18].  

For an alternate explanation: Pain Gate Theory Article Science Daily Physiotherapy Journal Article: Pain Theory & Physiotherapy

This model was the first to challenge the long-held assumptions of a biomedical approach to managing pain, and advancements in the understanding of anatomy, neurology and cognition have led to models fully incorporating the biopsychosocial model contemplating the reciprocal nature of mood and cognition on pain and vice versa. 

Biopsychosocial Model of Pain[edit | edit source]

There are a large number of different models to contemplate and only a few will be discussed here, links and references to others will be provided here

The biopsychosocial approach holds that the experience of pain is determined by the interaction between biological, psychological (e.g. cognition, behaviour, mood) and social (e.g. cultural) factors.[4]

This approach incorporates the view that perception of pain is influenced by the combination and interaction of biological, psychological and social factors (all of which can be broken down into different sub-categories). Not all models incorporate all three aspects, with some focusing mainly on behaviour.[19] It is important to consider that not one model is correct but that different models have strengths and weaknesses and suit patients on an individual basis.

As with all models, there is some difference of opinion with certain respects, such as which aspect has the greatest influence on pain perception. However, biopsychosocial models all agree on the central focus being not on a disease but on the behaviour around the disease, fueling beliefs and attitudes which can perpetuate the problem. The central argument, as stated, is illness behaviour which implies that individuals may differ in perception of a response to bodily sensations and changes (e.g. pain, nausea, heart palpitations), and that these differences can be understood in the context of psychological and social processes.[4]

Reconceptualising Pain[edit | edit source]

In the simplest evolutionary description pain is used to tell us that something is wrong or has been damaged and we need to change what we are doing.[20] In other words, pain, or nociception, gives an indication of current or impending damage to tissue. Effectively it is a protective mechanism to extend life and a crude form of learning from our mistakes. However, this 'simple mechanism' can develop into a more sinister and incorrect self-perpetuating cycle of chronic pain. There are a number of different ways the pain mechanism can go wrong.

Moseley proposes the following key points for reconceptualising pain and how pain serves our livelihood:[21]

1. Pain Does Not Provide a Measure of the State of The Tissues[21][edit | edit source]

Animal studies demonstrated that changes in behaviour were preceded by either tissue injury, or noxious stimulation. However, these pain behaviours, which could be as simple as a withdrawal reflex or more complex as time spent in a non-preferred versus a preferred environment, did not correspond proportionately to the stimulus.[21] This indicates an imprecise, inadequate measure of the state of the tissues.[21] Subsequent human studies illustrated that noxious stimulation does trigger nociceptor activity, but with a varying relationship between the nociceptor activation and pain ratings.[21]

2. Pain is Modulated By Many Factors From Across Somatic, Psychological and Social Domains[21][edit | edit source]

Some examples of physiological or social situations overcoming the effects of pain can be seen in the world of cycling. In the 2013 Tour de France, British Cyclist, Geraint Thomas was involved in a crash during the first stage of the race, resulting in a fractured pelvis as well as a large amount of soft tissue injury. Three weeks later he completed the Tour de France.[22] Other sporting examples include Tiger Woods who won the 2008 US Open with a torn ligament in his left knee and a double stress fracture in the same leg, or MotoGP world champion Jorge Lorenzo who finished fifth in a race despite undergoing surgery on a broken collarbone just one day prior to the race.[22] This ability to endure extreme pain through psychological and physiological determination in conjunction with limited medications available to elite sportsmen (due to fear/risk of a doping ban) has been studied by many researchers and has been summarised by Fields et al.[13] These findings are yet more evidence to show that pain is not simplistic or simply controlled or experienced by somatic mechanisms alone.

Studies investigating the influence of psychological context on the effects of pain often show the influential relationship between the two. One of the more extensively studied subjects is the influence of attention on pain and vice versa. Even though there is a  definitive amount of data on the subject, opinion is divided.[23] Some evidence suggests focusing on the pain intensifies it while other studies suggest the opposite.[24][25][26] The expectation of pain can also be a factor in the perception of pain. [27][28]

"As a general rule, expectation of a noxious stimulus increases pain if the cue signals a more intense or
more damaging stimulus and decreases pain if the cue signals a less intense or less damaging stimulus"[21]

3. The relationship between pain and the state of the tissues becomes less predictable as pain persists[21] [edit | edit source]

"...the neurones that transmit nociceptive input to the brain become sensitised as nociception persists, and... the
networks of neurons within the brain that evoke pain, become sensitised as pain persists."[21]

The idea of neuroplasticity and pain is well documented and can be used to explain the above statement by Moseley.[21][29][30] This may be the way in which allodynia and hyperalgesia occur. In simple terms (the way in which this author of this page explains it to his patients) when you play a video game, tennis or any task the more you practice the better you get. This is because your brain learns and adapts. The same can go for pain: the more you sense it, the more you focus on it the more of a central part of your life it becomes and you become super-sensitised to it which perpetuates the problem. 

Chronic Pain Management[edit | edit source]

Modern cognitive behavioural approaches to pain have developed from a number of linked models, all with some efficacy on their own but gaining from being delivered in combination. They have clearly been shown to be the most logical treatment for individuals suffering from chronic musculoskeletal pain, where the pain is accompanied by disability and psychological distress.

In essence, cognitive behavioural approaches aim to improve the way that an individual manages and copes with their pain, rather than finding a biological solution to the putative pathology. Chronic pain has been linked to increased mortality and dementia.[31] The approach is very much related to problem solving and returning control to the sufferer. Many patients state that the pain rules their lives and cannot see how this can change without a medical cure. However, with appropriate instruction in a range of pacing techniques, cognitive therapy to help identify negative thinking patterns and the development of effective challenges, stretching and exercising to improve physical function, careful planning of tasks and daily activities, and the judicious use of relaxation training, many people find the treatment enables them to take back control of their lives, to do more and feel better.

Educational strategies, such as Explaining Pain and Pain Neuroscience Education (PNE) have also been used to treat chronic pain.[32][33] The aim of educational strategies is to provide patients with an understanding of the biological processes behind pain in order to reduce pain.[33] The Explaining Pain approach highlights to a patient that pain is not a marker of tissue disease, but rather a sign of the perceived need to protect the body.[33] Pain Neuroscience Education (PNE) focuses on teaching people in pain about the neurobiology and neurophysiology of pain.[32] While the current evidence for Explaining Pain is low-level, the evidence base is growing and, clinically, it appears to offer improvements in pain and disability.[33] Similarly, PNE has been found to be effective in the treatment of chronic pain.[32]

Transcutaneous electric nerve stimulation (TENS) is thought to activate a complex neuronal network leading to a reduction in pain. Conventional TENS corresponds to the use of high frequency (100 Hz or more), low intensity and a short pulse duration (50–80 µs). This combination of parameters activates non-noxious afferent nerve fibers (Aβ fibers). The effect of such mode is traditionally attributed to the activation of these fibers thought to modulate Aδ and C fibre-mediated nociceptive transmission in the spinal cord. TENS can be proposed only when the size of the pain area is limited and when cutaneous sensitivity still exists, A better analgesia can probably be obtained with higher intensities but the patients must feel a comfortable tingling (with high frequency) or tapping (with low frequency) that should never be painful.[34]

Transcranial direct current stimulation (tDCS) is a type of electrical stimulation delivered continuously (“direct current”) for 20–30 min at a low intensity.[35] The analgesic effect of other forms of low-intensity electrical stimulation delivered transcranially, such as transcranial alternating current stimulation (tACS) or transcranial random noise stimulation (tRNS), has not been proven in neuropathic pain.[36][37]

Repetitive transcranial magnetic stimulation (rTMS), first described by Faraday in 1831 relies on electromagnetic induction. In practice, an rTMS session lasts about 15–30 min. The focal figure of 8 stimulation coil makes the use of a neuronavigation system that is helpful in allowing comparable and reproducible stimulation targeting between sessions, especially for non-motor cortical targets. Overall, the level of evidence is higher for rTMS compared to tDCS,[38] in part because the amount of data is larger for rTMS than for tDCS.[37]

Various invasive stimulation for neuromodulation such as Deep Brain Stimulation, Spinal Cord Stimulation, cortical stimulation, Dorsal root ganglion stimulation (DRG stimulation), Spheno‑palatine ganglion stimulation (SPGS), Occipital Nerve Stimulation (ONS) for neuropathic pain have been suggested for different conditions. However, the evidence is lacking for clinical usage.

Therapeutic exercise is associated with decreased pain complaints.

Assistive devices reduce stress on joints and help in reducing pain and improve overall function.

Manual therapy may be beneficial in the case of persistent pain with ongoing nociception.

Neuromuscular reeducation using EMG biofeedback can teach patients to relax overactive muscles and isolate functional muscles without over recruitment.

Exercise, multidisciplinary rehabilitation, acupuncture, Cognitive Behavorial Therapy, and mind-body practices were most consistently associated with durable slight to moderate improvements in function and pain for specific chronic pain conditions.[39]

References[edit | edit source]

  1. Sturgeon JA, Zautra A. Resilience: A New Paradigm for Adaptation to Chronic Pain. Current Pain and Headaches Reports. 2010; 14(2): 105-112.
  2. Goldberg DS, McGee SJ. Pain as a global public health priority. BMC public health. 2011 Dec;11(1):1-5.
  3. Barke A, Korwisi B, Jakob R, Konstanjsek N, Rief W, Treede RD. Classification of chronic pain for the International Classification of Diseases (ICD-11): results of the 2017 International WHO Field Testing. Pain. 2021 Apr 8.
  4. 4.0 4.1 4.2 4.3 4.4 Asmundson,G. Gomez-Perez,L. Richter, A. Carleton, RN. The psychology of pain: models and targets for comprehensive assessment. Chapter 4 in Hubert van Griensven’s Pain: A text book for health care professionals. Elsevier, 2014.
  5. Federation of State Medical Boards of the United States .Model guidelines for the use of controlled substances for the treatment of pain. The Federation, Euless, TX (1998)
  6. Merskey, H., Bogduk, N., 1994. Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms, second ed. IASP Press, Seattle
  7. International Association for the study of Pain (IASP). Classification of Chronic Pain, Second Edition (Revised). 2011. [ONLINE] Available from;navItemNumber=677
  8. Asmundson, G.J.G., Norton, G.R.,Allerdings, M.D., et al., 1998. Posttraumatic stress disorder and work-related injury. J. Anxiety Disord. 12, 57–69
  9. Turk, D.C., Rudy, T.E., 1987. IASP taxonomy of chronic pain syndromes: Preliminary assessment of reliability. Pain 30, 177–189
  10. Scholz J, Finnerup NB, Attal N, Aziz Q, Baron R, Bennett MI, Benoliel R, Cohen M, Cruccu G, Davis KD, Evers S. The IASP classification of chronic pain for ICD-11: chronic neuropathic pain. Pain. 2019 Jan;160(1):53.
  11. The British Pain Society. FAQs. [ONLINE] Accessed 13/03/2014 available from
  12. 12.0 12.1 12.2 12.3 Melzack R, Wall PD. Pain Mechanisms: A New Theory. Science: New Series 150. (1965:971-979)
  13. 13.0 13.1 Fields HL and Basbaum AI. Central Nervous System Mechanisms of Pain Modulation. in Wall Parkinson's and Melzack R (eds). Textbook of Pain. 1999: 309-330
  14. Jenkins G. Kemnitz C. Tortora G. Anatomy and Physiology: From Science to Life. New Jersey :John Wiley sons, Inc 2007
  15. Nagi SS, Marshall AG, Makdani A, Jarocka E, Liljencrantz J, Ridderström M, et al. An ultrafast system for signaling mechanical pain in human skin. Science Advances. 2019;5(7).
  16. Yam M, Loh Y, Tan C, Khadijah Adam S, Abdul Manan N, Basir R. General Pathways of Pain Sensation and the major neurotransmitters involved in pain regulation. International Journal of Molecular Sciences. 2018;19(8):2164.
  17. Martini, FH. Nath, JL. Fundamentals of Anatomy Physiology. (8th edn). San Francisco:Pearson. 2009
  18. Melzack, R., Casey, K.L., 1968. Sensory, motivational and central control determinants of pain. In: Kenshalo, D.R. (Ed.), The Skin Senses.fckLRCC Thomas, Springfield, IL, 423–439.
  19. Fordyce WE, Fowler RS, DeLateur B. An application of behavior modification technique to a problem of chronic pain. Behaviour Research and Therapy. 1968;6(1):105–7.
  20. The Science Museum. Why do we feel pain? [ONLINE] Accessed on 20/03/2014
  21. 21.0 21.1 21.2 21.3 21.4 21.5 21.6 21.7 21.8 21.9 Moseley GL. Reconceptualising pain according to modern pain science. Physical Therapy Reviews. 2007;12(3):169–78.
  22. 22.0 22.1 Beaven C. Hayles, R. Tour de France 2013: Geraint Thomas pain must be horrendous [ONLINE] Accessed 20/03/2104 available from:
  23. Asmundson GJ, Kuperos JL, Norton GR. Do patients with chronic pain selectively attend to pain-related information? Preliminary evidence for the mediating role of fear. Pain 1997;72:27–32
  24. Crombez G, Eccleston C, Baeyens F, Eelen P. Attentional disruption is enhanced by the threat of pain. Behav Res Ther 1998;36:195–204
  25. Eccleston C, Crombez G, Aldrich S, Stannard C. Attention and somatic awareness in chronic pain. Pain 1997;72:209–15
  26. Crombez G, Eccleston C, Baeyens F, van Houdenhove B, van den Broeck A. Attention to chronic pain is dependent upon pain-related fear. J Psychosom Res 1999;47:403–10
  27. Fields HL. Pain modulation: expectation, opioid analgesia and virtual pain. Biol Basis Mind Body Interact 2000:245–53
  28. Wager TD. Expectations and anxiety as mediators of placebo effects in pain. Pain 2005;115:225–6
  29. McMahon SB, Koltzenburg M. Wall and Melzack’s Textbook of Pain. London: Elsevier, 2006
  30. Butler D. The sensitive nervous system. Adelaide: NOI Publications, 2000
  31. Domenichiello AF, Ramsden CE. The silent epidemic of chronic pain in older adults. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2019 Jul 13;93:284-90.
  32. 32.0 32.1 32.2 Louw A, Nijs J, Puentedura EJ. A clinical perspective on a pain neuroscience education approach to manual therapy. J Man Manip There. 2017; 25(3): 160-168.
  33. 33.0 33.1 33.2 33.3 Moseley L, Butler,  DS. Fifteen years of explaining pain: the past, present and future. The Journal of Pain. 2015; 16(9): 807-813.
  34. Moran F, Leonard T, Hawthorne S, Hughes CM, McCrum-Gardner E, Johnson MI, et al. Hypoalgesia in response to transcutaneous electrical nerve stimulation (TENS) depends on stimulation intensity. The Journal of Pain. 2011;12(8):929–35.
  35. Moisset X, Lefaucheur J-P. Non pharmacological treatment for neuropathic pain: Invasive and non-invasive cortical stimulation. Revue Neurologique. 2019;175(1-2):51–8.
  36. Palm U, Chalah MA, Padberg F, Al-Ani T, Abdellaoui M, Sorel M, et al. Effects of transcranial random noise stimulation (trns) on affect, pain and attention in multiple sclerosis. Restorative Neurology and Neuroscience. 2016;34(2):189–99.
  37. 37.0 37.1 Moisset X, Lanteri-Minet M, Fontaine D. Neurostimulation methods in the treatment of chronic pain. Journal of Neural Transmission. 2020 Apr;127(4):673-86.
  38. Lafaucheur J-P, Cantello RM, Benninger DH, Baeken C, Ayache SS, Antal A, et al. Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS). Clinical Neurophysiology. 2014Nov;125(11):2150–206.
  39. Skelly AC, Chou R, Dettori JR, Turner JA, Friedly JL, Rundell SD, Fu R, Brodt ED, Wasson N, Winter C, Ferguson AJ. Noninvasive nonpharmacological treatment for chronic pain: a systematic review.
  40. Cleveland Clinic. Lifestyle Changes and Therapies to Manage Chronic Pain | William Welches, Do, PhD. Available from: [last accessed 19/8/2021]