Motivation and emotion/Book/2016/Chronic pain and negative emotion

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Chronic pain and negative emotion:
What are the negative emotional effects of chronic pain and how can these be managed?

Overview[edit | edit source]

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What is chronic pain? Does the experience of chronic pain cause people to feel negative emotions? Pain is experienced by most people however for some it becomes chronic, persistent and is unresponsive to medications. Frustration can arise when the cause cannot be found [grammar?] leaving some feeling stigmatised and vulnerable to negative emotions. This chapter will explore the theories of pain and their progression from purely physical to integrating mind and body. The experience of stigma will be discussed and the relationship between chronic pain and negative emotions will be explored focusing on anxiety and depression. The most popular treatment options are introduced with emphasis on an interdisciplinary approach.

Definitions[edit | edit source]

"Approximately 1 in 5 Australians are living in chronic pain"

(Pain Management Research Institute, 2011)

  • Pain is considered chronic or persistent when still being experienced more than three months after the initial injury.
  • Has failed to respond to standard medications; and
  • Negative affective and behavioural changes have occurred.

Watch this TED Talk presented by Elliot Krane: The mystery of chronic pain

What is negative emotion? Negative emotion is an unpleasant or unhappy mood and includes a variety of emotions including anger, sadness, guilt, fear and nervousness. These emotions are often expressed within the context of the psychological conditions anxiety and depression.

Types of chronic pain and locations[edit | edit source]

Table 1.

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Neuropathic Pain
  • Location - central nervous system (brain & spinal cord), peripheral nerves
  • Sensation - burning, shooting, stabbing, pulsing, heavy sensation
  • Damage or injury to nerves
Nociceptive Pain
  • Location - visercal and somatic
  • Sensation - sharp, aching, throbbing
  • Damage to body tissue e.g. mechanical injury, cancer, benign tumour

Neuropathic & Nociceptive Pain

  • Location - central nervous system (brain & spinal cord), peripheral nerves and visercal and somatic
  • Sensation - sharp, aching, throbbing, burning, shooting, stabbing, pulsing, heavy sensation
  • Damage to body tissue e.g. mechanical injury, cancer, benign tumour and/or damage or injury to nerves

Common chronic pain complaints:

lower back pain, migraines, rheumatoid arthritis, complex regional pain syndrome, chronic fatigue syndrome, phantom limb pain, neuropathy,

conversion disorder, foot and leg pain, fibromyalgia and post surgical pain

Symptoms of chronic pain[edit | edit source]

Physical Symptoms Negative Emotions & Associated Problems
  • Mild to severe pain that does not go away
  • Pain that may be described as shooting, burning, aching, or electrical
  • Feeling of discomfort, soreness, tightness, or stiffness
  • Changes in mood including hopelessness, fear, depression, irritability, anxiety and stress
  • Sleeplessness
  • Fatigue
  • Withdrawal from activity and increased need to rest        
  • Weakened immune system
  • Disability

Mini Quiz 1- About chronic pain.
Now that you have read the basics why not test yourself.

1 What percentage of Australians suffer from chronic pain?


2 What is the definition of chronic pain?

Persistent for more than 3 months
Failed to respond to medications
Negative affect and behaviour changes
All of the above

Historical context of understanding pain[edit | edit source]

Figure 2. Illustration of Descartes pain pathway

Several theoretical frameworks have emerged to explain the physiological and psychological basis of pain but as yet none completely accounts for all aspects of pain perception. Rene Descartes in his Treatise of Man 1664 took pain from being a mystical event to something mechanical theorising that pain travelled from its point of origin along nerve fibres until it reached the brain. This notion revolutionised the concept of pain from an uncontrollable event attributed to god or magic to one that potentially could be halted (Asmundson & Wright, 2004). What transpired from this insightful inference were multiple mechanistic models which attempted to locate 'pain generators' and therefore focused on the physical and tangible aspects of pain. These models could account for acute pain but had major limitations in explaining chronic pain. Until Melzack and Wall introduced the Gate Control Theory which revolutionised the field of pain by assigning the central nervous system a role greater than mere receiver of information and introduced the concept of pain being more than the sum of its parts (Melzack & Katz, 2004). They later developed the Neuromatrix pain theory as they began to understand the significance of body-mind connection and the interplay of physiological, endocrinology, autonomic nervous system, psychological and social factors. This led to a plethora of biopsychosocial theories that led to the emergent understanding that chronic pain is more than just acute pain that has not subsided. However, the impact of the original mechanistic models cannot be understated as physicians can still be found practising the principle of tissue damage equates to pain sensation (Holloway, Sofaer-Bennett, & Walker, 2007).

Theories of pain[edit | edit source]

[Provide more detail]

The body as machine[edit | edit source]

Much of western medicine is mechanistic meaning that the body is treated in parts rather than as a whole system. This concept is strongly entrenched in the psyche of many medical professionals due to teaching models' reliance on these early pain models. The health community reflects this with multiple specialists (e.g. psychologists, psychiatrists, rheumatologists). This approach often leads chronic pain sufferers feeling frustrated and disappointed as they are referred to many different professionals without resolution of management of their pain.

The following theories highlight the progression and development of the reductionist model:

The specificity of pain theory (1800s)[edit | edit source]

Specificity theory is one of the first modern theories of pain. It proposed that tissue damage activated specific pain receptors in the body and nerve fibres then transmitted pain signals to a 'pain centre' in the brain via the spinal cord. Pain is therefore proportional to the amount of tissue damage or pathology experienced and was wholly considered a peripheral phenomenon. This theory excluded psychological contributions to pain such as anxiety, depression or past experience. If patients continued to suffer chronic pain after the healing process they were considered psychologically impaired and referred to psychiatrists (Moayedi & Davis, 2013).

Pattern theory (1955)[edit | edit source]

Pattern theory was developed in opposition to the specificity of pain theory and ignored the evidence of specific receptors. Theorists proposed that all skin receptors with the exception of innervating hair cells are identical. It was believed that sensations were transmitted by a unique pattern of neural firing which then became encoded for intensity and stimulus type. Like the specificity of pain theory psychological contributors were ignored however it is noted that pattern theory potentially set the stage for gate control theory (Moayedi & Davis, 2013).

Gate control theory (1965)[edit | edit source]

The psychologist Ronald Melzack and physiologist Patrick Wall proposed this theory in response to the limitations of specificity theory and pattern theory. The gate control theory of pain proposes that nerve impulses from afferent (sensory) nerve fibres to the spinal cord transmission cells (T-cells) are controlled by a gating mechanism in the spinal dorsal horn. Large and small nerve fibres influence the gating mechanism with large fibres tending to inhibit transmission (close the gate) and small fibres facilitating transmission (open the gate). The small nerve fibres transmit pain and the large nerve fibres transmit touch, pressure and other skin sensations.The gating mechanism is also influenced by descending nerve impulses sending messages from the brain. It is believed that when the spinal cord (T-cells) are stimulated beyond the critical level it activates complex neural patterns which gives the experience of pain (Carli, 2011).

The contribution of this theory to understanding pain cannot be understated as it emphasised the central nervous system as an active system that filters, selects and modulates information rather than a passive receiver and introduced the notion that affect, motivation and past experience are compatible with the pain experience (Carli, 2011; Melzack, 1999).

The mind-body connection[edit | edit source]

The connection between mind and body was a significant milestone in the understanding of chronic pain introducing the concept of emotion into the experience of pain rather than it being entirely related to tissue damage or inflammation.

Neuromatrix pain theory[edit | edit source]

The neuromatrix pain theory is a theoretical model proposed by Melzack in response to the limitations of the gate control theory and explores linking pain to more than injury, inflammation or other tissue pathology. Melzack recognised that the gate control theory could not explain the sensation of pain in the absence of injury such as phantom limb pain which implicates the involvement of neural activities in the sensation of pain (Melzack, 2001). He proposed the neuromatrix which is a distributed network of neurons that generates patterns and processes transmitted information that then produces the body-self with changing perceptual and emotional experiences. Pain is described as a multidimensional experience influenced by genetic vulnerabilities, sensory factors and neural-hormone mechanisms with stress being identified as a major contributor (Melzack & Katz, 2004).

Biopsychosocial approach to chronic pain[edit | edit source]

Figure 3. The Biopsychosocial Model of Health

The biopsychosocial approach to chronic pain posits that pain is an interaction between biological, psychological and social factors. These factors include tissue damage, nervous system involvement, cognition, affect and behaviour; social and cultural influences. This broad and multi-dimensional model is theoretically sound however it is difficult for medical professionals to access such broad data that is reliable about their patients (Suls & Rothman, 2004). The theories listed below have attempted to conceptualise chronic pain within the three factor framework.

Asmundson & Wright (2004) explained the following theories regarding chronic pain:

The operant model[edit | edit source]

This model details how operant conditioning through positive and negative reinforcement serves as a mechanism by which acute pain behaviours become chronic. Escape, withdrawal or avoidance behaviours are used adaptively to reduce further tissue damage and therefore reduce further pain and suffering. Prolonged maladaptive behaviour is then reinforced by increased social attention from friends and family and reduction of personal responsibility. Chronic pain continues after pathology has healed and results in increased dependence on medication, others and possible development of additional illnesses.

The Glasgow model[edit | edit source]

The Glasgow Model applied illness behaviour to chronic back pain believing it stems from physiological impairment and is influenced by cognition, affect and social factors. The model emphasises physical impairment as an important antecedent to further pain that is distinct from the original injury.

Fear-avoidance models[edit | edit source]

Fear-avoidance models came from observation of the considerable anxiety experienced by sufferers and was influenced by operant conditioning models. Once an injury has occurred it is appraised as either non-threatening or threatening; if considered non-threatening then it is easily overcome [grammar?] however if considered threatening then maladaptive behaviours and cognition can induce a fear-avoidance cycle that can result in undesirable consequences both physical and psychological. Like the Glasgow model [grammar?] further pain distinct from the original location tends to be suffered.

Diathesis-stress model[edit | edit source]

This model incorporates physiological, psychological, and sociocultural factors in the cause, exacerbation, and maintenance of chronic pain. It recognises that an initial injury sets off an appraisal process and those with predispositional vulnerabilities tend to become distressed resulting in a fear response and oversensitivity to physical symptoms. This leads to cognitive and behaviour changes of anxious preparedness and an involvement of the autonomic nervous system. The impact of the original injury declines but the learning process sets up a cycle of anxious anticipation of events only remotely associated with pain.

Mini Quiz 2 - Theories of pain.
Now that you have read the basics why not test yourself.

1 If Jane's doctor asked questions about coping, mood, family and physical symptoms what approach is she using?

The Specificity of Pain Theory
Reductionist Approach
Biopsychosocial Approach
The Gate Control Theory

2 If Jane had x-rays and MRIs to locate an injury or inflammation for her chronic pain what approach is being used?

Body as Machine
Mind-Body Connection

Stigma of chronic pain[edit | edit source]

Figure 3. Stigma of chronic illness and feeling like a hyperchondriac

"When you have been in pain for a long time, you don't actually see the consultant. You wait for ages and ages and ages and you come out feeling totally baffled really. He [the doctor] doesn't really seem to understand your problem and you feel like bursting into tears, you have wasted such a lot of time and energy ... You don't feel that you're being treated like a person at all''

Judith (aged 58) p.1458

Research by De Ruddere, Bosmans, Crombez and Goubert (2016) indicates that individuals suffering from chronic pain are vulnerable to stigmatisation by others. They define stigma as the devaluing and discrediting of responses from individuals who for some reason deviate from a norm. Chronic pain sufferers can feel stigmatised when the cause of their pain is left undetermined even when thoroughly investigated by medical tests and countless specialist appointments. Often feeling judged and labelled as malingers sufferers can become frustrated and disappointed in the medical system as evidenced by the following experiences:

"I’ve got the pain and nobody can point to anything and that’s why people can say is it up in his head” Steve (44)

“Society in general will think I am making excuses ... I haven’t got anything they can actually see” Carol (38)

“... her manner didn’t help; very very dismissive and very sort of abrupt ... she didn’t do anything for me" Jane (after visiting a neurosurgeon)

(Holloway et al., 2007 p.1459 -1460 )

This disregard or anticipation of negative social reactions can begin to affect one’s self-concept (De Ruddere et al., 2016). Self-concept is the individual’s belief about themselves and their attributes (Baumeister, 1999) and having chronic pain can relegate an individual to the "sick role" (Holloway et al., 2007). If the "sick role" is assigned to the patient then it is the task of medicine to treat and cure the patient and when this does not occur then medical staff can appear indifferent, further exacerbating the sense of stigma (Holloway, et al., 2007).

Social interactions are essential to the development of self-concept and any form of social isolation is directly related to lower psychological well-being (De Ruddere et al., 2016). This links to another important concept known as 'relatedness' [grammar?] it has been identified that everyone has an innate need to form emotional attachments that satisfy our need to be liked and accepted it is also essential to our psychological health (Reeve, 2015). This is concerning given a study done by De Ruddere et al., (2016) found that health care professionals and the general population felt less sympathy for patients with unexplained pain and were less inclined to help.

Holloway et al., (2007) found the following in their study of chronic back pain that stigmatising can also occur in places of employment where chronic pain sufferers can be terminated due to days off work or find themselves unemployable due to limited ability to undertake physical activity or inability to sit for long periods. With some chronic pain sufferers reporting that others believed they were using their chronic pain as an agent to scam money from benefits [grammar?]. It can also lead some to under report their pain levels and distress and potentially exacerbate their chronic pain so they do not lose their financial security.

Even significant others can become suspicious of their spouse's chronic pain especially when it is without a diagnosis [grammar?] often spouses are shouldering the larger share of household duties whilst juggling work demands. Some chronic pain sufferers will hide the extent of their suffering in fear that they may damage their relationship.

Finally [grammar?] it is not surprising that (Holloway, et al., 2007) found that depression is congruent with feelings of inadequacy and shame as a result of being stigmatised[Provide more detail].

Chronic pain, anxiety and depression[edit | edit source]

Figure 4. Many chronic pain sufferers feel depressed

Chronic pain has a negative impact on social, physical and psychological well-being and is a risk factor for developing anxiety and depressive disorders (Gerrits et al., 2014; Lame, Peters, Vlaeyen, Kleef, & Patijin, 2005). The biopsychosocial approach has been used in a number of studies to understand the connection between chronic pain, anxiety and depression. The pain-avoidance model suggests that catastrophic thinking and hypervigilance contributes significantly to chronic pain. Catastrophic thinking is an exaggerated negative response towards pain and pain stimuli and hypervigilance is selective attention given to particular bodily sensations and then appraised negatively (Wood, Chow, Chen, Lim et al, 2014). Together [grammar?] these maladaptive thoughts lead to avoidance behaviours which limit mobility, social excursions and contribute to disability and fearful thinking.

Lucchetti, Oliveira, Mercante, & Peres (2012) found that high anxiety levels lead to more severe and long lasting pain and more cases of chronification for migraine sufferers. They believe this could be caused by the extended periods of muscle tension reported by anxiety sufferers. They also report that there appears to be a connection between people suffering anxiety and chronic pain as those with anxiety often have lower pain tolerance than those without anxiety.

Studies have shown that people in chronic pain often have sleep disturbances [grammar?] either sleep latency or multiple waking during the night (van de Water, Eadie, & Hurley, 2011). Although this does not cause anxiety or depression [grammar?] the reduced quality of sleep has a negative impact on mood, occupational functioning and well-being. The sleep deprivation can also lower pain thresholds and mental capacities.

Depression or a depressed mood is common in people experiencing chronic pain [grammar?] often exacerbating disability and worsening overall quality of life (Williams & Schafer, 2016). It is accepted that even though chronic pain and depression present as comorbid conditions [grammar?] it is the chronic pain that predisposes the patient to depression rather than depression to chronic pain (Ryan & McGuire, 2016). Although this link is commonly expressed in literature [grammar?] the exact relationship between chronic pain and depression is unknown [grammar?] however a number of theories have been developed.

Ryan & McGuire (2016) have explained the relationship between chronic pain, depression and anxiety within the self-determination theory and self-concealment. Self-determination theory refers to three needs that are considered essential for psychological well-being; autonomy, relatedness and competence and self-concealment is the tendency for chronic pain sufferers to hide the full-extent of their pain experience. The motivation of self-concealment is for chronic pain sufferers to maintain a healthy current self-image. Whilst attempting to achieve these needs (and therefore psychological health) patients begin to feel controlled and constrained by having to deceive others (e.g. concealing medical appointments; hiding pill taking) which results in lowered pain tolerance and higher self-reported pain levels. The mechanism of self-concealment to uphold the three psychological needs ultimately leads to feelings of depression and anxiety as chronic pain sufferers find it increasingly difficult to cope and maintain the self-imposed facade of wellness.

The co-morbid presentation of depression and chronic pain has led to multiple biological theories which suggest a common underlying mechanism. Currently the mechanism is unclear but researchers have studied dysfunction in the serotonin and noradrenline pathways (Stahl & Briley, 2004), involvement of the hypothalamus-pituitary-adrenal axis (Blackburn-Monro, 2004), and limbic system neuroplasticity (Gonclaves et al., 2008). All of these biological mechanisms show promise [grammar?] however most research involves animal rather than human models and further investigation is required.

Treatments[edit | edit source]

[Provide more detail]

Pharmacological[edit | edit source]

All drugs have more than one effect beside the desired one. Non-desired effects are called side-effects and which can cause unpleasant symptoms like constipation, drowsiness, nausea, vomiting and rashes.

Table 2.

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Analgesics Anti-Inflammatories Adjuncts for Wellness
  • Mild - paracetamol, aspirin
  • Moderate - codeine, mixed codeine & paracetamol
  • Severe - opoids e.g. morphine, fentanyl
  • Non-steroidal (NSAIDS) - ibuprofen, meloxicam
  • Corticosteroids - prednisone, dexamethasone
  • Anti-depressants - citalopram, paroxetine
  • Tranquilisers - valium, ativan
  • Sleeping Tablets - doxylamine, phenergan

Research has shown that pharmacological interventions are often unsuccessful in the treatment of chronic pain due to its multi-dimensional characteristics therefore alternative treatments need to be prescribed (Kuijpers et al., 2010).

Transcutaneous electrical nerve stimulation (TENS)[edit | edit source]

Figure 5. TENS pain relieving device.

Transcutaneous electrical nerve stimulation (TENS) is a relatively non-invasive intervention to treat pain [grammar?] it is believed to be safe and reasonably effective[factual?]. It is used to alleviate different sorts of pain including back pain, surgical pain, neuropathic pain and migraines (Carroll, Moore, McQuay, Fairman, Tramer, & Leijon, 2008). Reports have shown that TENS reduces pain by both peripheral and central nervous system mechanisms. Studies have had mixed results for chronic lower back pain but this could be due to methodology issues (De Santana, Walsh, Vance, Rakel, & Sluka, 2008).

One criticism of TENS is that it relies on the mechanistic treatment style and does not recognise or treat negative emotions or the psychological conditions which often are experienced by chronic pain sufferers.

Interdisciplinary treatment approach[edit | edit source]

An interdisciplinary approach to chronic pain management has been found to be an effective treatment method. Commonly this will include health psychology, medication management, and physical therapy all within a cognitive behaviour framework (Institute of Chronic Pain, 2016 ).

Listening and believing the patient are very important in the therapeutic process and dealing with stigma should be included as part of the cognitive behavioural therapy (CBT) program (Holloway et al., 2007). The emphasis of chronic pain management has started to shift towards self-management with the most important outcome to be a return to work and improvement in functions and pain reduction (Holloway et al., 2007).

The goals of CBT are to reduce pain and psychological distress by decreasing maladaptive behaviours, increasing adaptive behaviours and identifying and correcting dysfunctional thoughts and beliefs and increasing self-efficacy for pain management (Ehde, et al., 2014). Studies has[grammar?] shown that of the dysfunctional thoughts pain catastrophising and hypervigilance are the most strongly correlated and therefore require added attention to resolving (Lame, Peters, Vlaeyen, Kleef, & Patijin, 2004).

CBT for chronic pain tends to be conducted one-on-one with session numbers depending on progress and financial pressures. Techniques include relaxation training, identifying behavioural goals (e.g. exercise or physical therapy), guidance in activity pacing, problem solving and cognitive restructuring (Ehde, et al., 2014).

Conclusion[edit | edit source]

Chronic pain is more than acute pain that has just not gone away. It is persistent, unresponsive to medications and negatively affects emotions and behaviours. The early pain theories captured the understanding of acute pain rather well [grammar?] however it was not until the theories were expanded to include all of the human experience; biological, psychological and social that chronic pain started to be understood. Nonetheless{g}} the early models created a lasting impression on the medical professionals and have led to chronic pain sufferers feeling stigmatised. The pervasiveness of chronic pain can lead vulnerable patients to have dysfunctional and maladaptive thoughts, feelings and behaviours which may transform into anxiety and depression. Standard pharmacological medications for chronic pain often fail therefore other options have been explored with an interdisciplinary approach being favoured due to its inclusive methodology.

See also[edit | edit source]

References[edit | edit source]

Asmundson, G., & Wright, K. (2004). Biopsychosocial approaches to pain. In T. Hadjistavropoulos & K. Craig (Eds.), Pain Psychological Perspectives (pp. 35-58). Mahwah, New Jersey: Lawrence Erlbaum Associates.

Blackburn-Munro, G. (2004). Hypothalamo-pituitary-adrenal axis dysfunction as a contributory factor to chronic pain and depression. Current Pain and Headache Reports, 8(2), 116-124.

Carli, G. (2011). Historical perspective and modern views on pain physiology: from psychogenic pain to hyperalgesic priming. Archives Italiennes de Biologie, 149(suppl.). 175-186.

Carroll, D., Moore, R., McQuay, H., Fairman, F., Tramèr, M., & Leijon, G. (2000) Transcutaneous electrical nerve stimulation (TENS) for chronic pain. Cochrane Database of Systematic Reviews 2000, doi: 10.1002/14651858.

DeRuddere, L., Bosmans, M., Crombez, G., & Goubert, L. (2016). Patients are socially excluded when their pain has no medical explanation. American Pain Society, 17(9). 1028-1035.

DeSantana, J,. Walsh, D., Vance, C., Rakel, B., & Sluka, K. (2008). Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain. Current Rheumatology Journal, 10(6), 492-499.

Ehde, D., Dillworth, T., & Turner, J. (2014). Cognitive-behavioural therapy for individuals with chronic pain: efficacy, innovations, and directions for research. American Psychologist, 69(2), doi: 10.1037/a0035747.

Gonclaves, L., Silva, R., Pinto-Ribeiro, F., Pego, J., Bessa, J., Pertovaara, A,... Almeida, A. (2008). Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of a rat. Experimental Neurology, 213(1), 48-56.

Holloway, I., Sofaer-Bennett, B., & Walker J. (2007). The stigmatisation of people with chronic pain. Disability and Rehabilitation, 29(18), 1456-1464.

Institute for Chronic Pain. (2014). What is a chronic pain rehabilitation program? Retrieved from

Kuijpers, T., van Middelkoop, M., Rubinstein, S., Ostelo, R., Verhagen, A., Koes, B., & van Tulder, M. (2011). A systematic review on the effectiveness of pharmacological interventions for chronic non-specific low-back pain. European Spinal Journal, 20(1). 40-50. doi: 10.1007/s00586-010-1541-4.

Lame, I., Peters, M., Vlaeyen, J., Kleef, M., & Patijn, J. (2005). Quality of life in chronic pain is more associated with beliefs about pain, than with pain intensity. European Journal of Pain, 9(1), 15-24.

Lucchetti, A., Oliveira, J., Mercante, J., & Peres, M. (2012). Anxiety and fear-avoidance in musculoskeletal pain. Current Pain and Headache Report, 16(5). 399-406.

Melzack, R. (1999). From the gate to the neuromatrix. Pain Supplement, 6(suppl.). 121-126.

Melzack, R. (2001). Pain and the neuromatrix in the brain. Journal of Dental Education. 65(12), 1378-1382.

Melzack, R., & Katz, J. (2004). The Gate Control Theory: Reaching for the brain. In T. Hadjistavropoulos & K. Craig (Eds.), Pain Psychological Perspectives (pp.13-34). Mahwah, New Jersey: Lawrence Erlbaum Associates.

Moayedi, M., & Davis, K. (2013). Theories of pain: from specificity to gate control. Journal of Neurophysiology, 109(1), doi: 10.1152/jn.00457.2012.

Pain Management Research Institute. (2014). About pain – Who suffers from pain. Retrieved from the University of Sydney website:

Reeve, J. (2015). Understanding Motivation & Emotion (6th ed.). USA:Wiley

Ryan, S. & McQuire, B. (2016). Psychological predictors of pain severity, pain interference, depression, and anxiety in rheumatoid arthritis patients with chronic pain. British Journal of Health Psychology, 21(2), 336-350.

Stahl, S., & Briley, M. (2004). Understanding pain in depression. Human Psychopharmacology, 19(S1), 9-13.

Suls, J., & Rothman, A. (2004). Evolution of the Biopsychosocial Model: Prospects and Challenges for Health Psychology. Health Psychology, 23(2), 119-125 doi: 10.1037/0278-6133.23.2.119.

van de Water, A., Eadie, J., & Hurley, D. (2011). Investigation of sleep disturbance in chronic low back pain: An age- and gender-matched case control study over a 7 night period. Manual Therapy, 16(6), 550-556.

Williams, A. & Schafer, G. (2016). How do we understand depression in people with persistent pain? Journal of Contemporary Psychotherapy, 46(3), 149-157.

Wong, W., Lam, H., Chow, Y., Chen, P., Lim, H., Wong, S. & Fielding, R. (2014). The effects of anxiety sensitivity, pain hypervigilance, and pain catastrophizing on quality of life outcomes of patients with chronic pain: a preliminary, cross-sectional analysis. Quality of Life Research, 23(8), 2333-2341.

External links[edit | edit source]