Chronic Pain

Original Editor - Scott Buxton

Top Contributors - Laura Ritchie, Rachael Lowe, Evan Thomas and George Prudden

Chronic Pain Explained

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 problem is that matters get worse not solely due to progression of the disease (the pathology in the tissues) but to the vicious circle the people find themselves in. A person who has pain, especially on movement, tends to avoid doing things that provoke their symptoms. They rest but unfortunately this is not a helpful treatment as it leads to secondary stiffness and weakness, causing worsening of the symptom that the individual is trying to avoid.

Inability to function leads to a loss of role and self-esteem with the progressive intrusion of other problems such as financial hardship and strained relationships. Tablets may cause side-effects, pain may prevent sleep, and all these difficulties cause worry and low mood which worsens the situation yet further. Treatments will be attempted through desperation rather than evidence of their 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

Previously pain used to fit into the biomedical model with a reductionist view (i.e Pain was derived from a specific physical pathology) and catagorically dismissed social, psychological and behavioural mechanisms as irrelevent and of no importance to understanding pain[1]. This is grossly oversimplified and now we understand that pain is more than a simple response to a physical stimulus and 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[2].

As the definition states, acute pain is a predicted response to a stimulus. If you have had surgery to repair and fractured hip, there will be a usual pattern of pain and rate of recovery based upon the patients 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 limiting to, intensity, quality, time course and personal meaning[3]

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[4] and, while not necessarily maladaptive[5][6], often leads to physical decline, limited functional ability and emotional distress.

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, for example common chronic pain problems cost the U.S.A US$60 billion per year[1] and in the UK somewhere in the region of £5 billion per year[7] and there are millions of lost work days throughout the world subsequently it is a crucial area in which treatment and management is continually being developed.

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Key Models to Understand Pain

Pain Gate Theory

The pain gate theory (PGT) was first proposed in 1965 by Melzack and Wall[9], 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[1]. 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 of transmission of noxious stimuli[10].

  1. α-Beta fibres - Large diameter and myelinated - Sharp pain - Faster
  2. α-Delta fibres - Small diameter and myelinated - Vibration and light touch - Fast
  3. C fibres - Small diameter and un-myelinated - 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 α-Beta fibres are the quickest of the 3 types followed by α-Delta fibres and finally C fibres[11].

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 α-Delta fibres are purely sensory in terms of touch. 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[12]. In the spinal cord there are also inhibitory interneurons which act as the 'gate keeper'. When there is no sensation from the nerves the inhibitory interneurons stop signals travelling up the spinal cord as there is no important information needing to reach the brain so the gate is 'closed'[9]. When the smaller fibres are stimulated the inhibitory interneurons do not act, so the gate is 'open' and pain is sensed. When the larger α-Delta fibres are stimulated they reach the inhibitory interneurons faster and, as larger fibres inhibit the interneuron from working, 'close' the gate. This is why after you have stubbed your toe, or bumped your head, rubbing it helps as you are stimulating the α-Delta fibres which close the gate[9]

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[13].  

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 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 Models of Pain

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[1].

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, some focus mainly on behaviour such as Fordyce et al. 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 on opinion with certain respects, such as which aspect has the greatest influence on pain perception, however biopsychosocial models all agree on the central focus; the focus is not on a disease but on the behaviour around the disease, feeding and fueling beliefs and attitude which perpetuates a problem. The central argument, as stated, is illness behaviour which implies that individuals may differ in perception of an 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[1].


Pain as a reflection on the Current State of a Persons Tissues

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[14]. Effectively it is a protective mechanism to extend life and a crude for of learning from our mistakes. However this can go wrong and 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.

The work of Lorimir Moseley and others have helped develop our knowledge of chronic pain and developed our understanding of pain from a biopsychosocial perspective.

In Moseleys' paper "Reconceptualising Pain According to Modern Pain Science" he argues several points[15]

That pain does not provide a measure of the state of the tissues

This can be argued because of the nature of early experiments attempting to measure pain only measuring simple observational behaviours such as a reflex or a more complex variable such as the amount of time spent in a non-preferred environment. These only show that a noxious stimulation changes behaviour and that neither behaviour or nerve activity explicitly explain or give you the true state of the tissues[15]. This is complicated further when the responses of different nerve fibres are measured as the complex nature of each nerve and their interlinking nature means it is very challenging to explain their relationship and influence on tissues.

That pain is modulated by many factors from across somatic, psychological and social domains

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 on stage one which resulted in a fractured pelvis as well as a large amount of soft tissue injury, 3 weeks later he completed the tour de france[16]. 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 rode a a race and finish fifth despite undergoing surgery on a broken collarbone the day previously[16]. 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[10]. These findings is 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 influencial relationship between the two. One of the more extensively studies 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[17]. Some evidence suggests focussing on the pain intensifies it but others suggesting the opposite however the association is clear[18][19][20].  Expectation of pain is also an area of study according to Moseley:

"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[15]"

A review of evidence about expectation and pain is written by Fields et al[21] and by Wager [22].

That the relationship between pain and the state of the tissues becomes less predictable as pain persists 

"...the neurones that transmit nociceptive input to the brain become sensitised as nociception persists, and that the
networks of neurons within the brain that evoke pain, become sensitised as pain persists[15]."

The idea of neuroplasticity and pain is well documented and can be used to explain the above quote[15][23][24]. 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 videogame, 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

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. 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.


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References

  1. 1.0 1.1 1.2 1.3 1.4 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.
  2. 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)
  3. Merskey, H., Bogduk, N., 1994. Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms, second ed. IASP Press, Seattle
  4. International Association for the study of Pain (IASP). Classification of Chronic Pain, Second Edition (Revised). 2011. [ONLINE] Available from http://www.iasp-pain.org/PublicationsNews/Content.aspx?ItemNumber=1673;navItemNumber=677
  5. 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
  6. Turk, D.C., Rudy, T.E., 1987. IASP taxonomy of chronic pain syndromes: Preliminary assessment of reliability. Pain 30, 177–189
  7. The British Pain Society. FAQs. [ONLINE] Accessed 13/03/2014 available from http://www.britishpainsociety.org/media_faq.htm
  8. All of These Videos. Chronic Pain - Explained. Available from: http://www.youtube.com/watch?v=B2SI-gmpDUU [last accessed 22/11/15]
  9. 9.0 9.1 9.2 Melzack R, Wall PD. Pain Mechanisms: A New Theory. Science: New Series 150. (1965:971-979)
  10. 10.0 10.1 Fields HL and Basbaum AI. Central Nervous System Mechanisms of Pain Modulation. in Wall PD and Melzack R (eds). Textbook of Pain. 1999: 309-330
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  14. The Science Museum. Why do we feel pain? [ONLINE] Accessed on 20/03/2014 http://www.sciencemuseum.org.uk/whoami/findoutmore/yourbrain/whatareyoursenses/whereareyou/whydowefeelpain.aspx
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  21. Fields HL. Pain modulation: expectation, opioid analgesia and virtual pain. Biol Basis Mind Body Interact 2000:245–53
  22. Wager TD. Expectations and anxiety as mediators of placebo effects in pain. Pain 2005;115:225–6
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