Psychology of Pain

Overview of Psychology of Pain
Cursory overview of pain psychology by Dr. Beth Darnall,
a Clinical Associate Professor in the Division of Pain Medicine at Stanford University

The psychology of pain is the study of the nociceptive (pain) experience, and the intricate interplay between the experience and an individual’s higher cognitive functions. It has been previously shown that while the body physiologically responds to painful stimuli, there are also higher brain areas that respond to pain to produce behavioural responses to minimize or avoid damage to the body [1]. Pain can affect the higher cognitive processing in a bottom-up manner, disrupting attention in the short term and possibly causing depression or hyper-vigilance in the long term [2]. On the other hand, the higher cognitive abilities can in turn affect the experience of pain by modulating its intensity. This can be from expectation, like the well-known placebo and nocebo effects [3], as well as from emotions that the individual is feeling. The importance of a patient’s mental state with respect to pain is stressed by the argument that the fear of pain can be more debilitating than the pain itself [2]. Consequently, the study of pain psychology yields valuable information in planning pain management in clinical settings.

1. Pain response models

1.1 Two-Part Model for Pain behavior

Two-Part Model for Pain behavior
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Differentiation of 2 types of pain responses: basic and advanced
Adapted from Meir et al. 2012 [6]

There seem to be two fundamentally different categories of pain responses present in humans. One is a basic response system involving physiological and bodily reactions, including change in facial colour or irregularities in breathing such as holding one’s breath or gasping, processed by the anterior-posterior insula[4],[5]. The other category is the advanced response system involving processing of pain signaling in higher brain centers initiating at anterior cingulate cortex (ACC)[4],[5]. This results in vocal, emotional, facial or protective reactions[6]. Vocal responses included moaning, crying and screaming (3 intensity levels); emotional responses included agitation, non-cooperation and irritability; facial responses included furrowing of eyebrows, squinting, and frowning; and finally, protective reactions included guarding the painful area, and moving it away[7]. This model was developed using metrics from the Non-communicating Adult’s Pain Checklist (NCAPC) for individuals with intellectual and developmental disabilities (IDDs). Thus, the metrics used to measure pain were by no means exhaustive, and some of the most complex or non-immediate behavioural responses may be missing from the list of responses in model.

1.2 Analgesic Problem Solving Model

Analgesic Problem Solving Model
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When an individual feels pain, their attention is interrupted and oriented
towards the pain. This puts them in a state of worry that then causes them to
try to solve the problem and seek analgesia. If a solution fails, then individuals
tackle the problem again as shown by the perseverance loop.
This may be harmful in chronic pain situations.
Modified and adapted from Eccleston and Crombez 2007 [9]

As pain is a noxious stimuli, it is reasonable that individuals feeling pain will try to avoid further pain, for example, by immobilizing a sprained ankle. Individuals will also seek analgesia whether that be by means of pharmaceutical analgesics or other treatments. This response begins with the interruption of the individual’s attention to cause worry which in turn promotes successful problem solving behavior[8]. The problem solving behavior involves characterizing the pain, trying to deduce the cause of the pain usually in biomedical terms then trying to seek ways to reduce or eliminate the pain. If the chosen solution fails, then the pain is redefined to find another solution and this loop continues until analgesia is found[1],[9].

Since worry is an element of a mechanism to promote successful problem solving, when there is no possible successful solution and repeated attempts at solution as failed, such as for chronic pain, it may be expected that worry would be extinguished. However, failed attempts only serve to increase worry which may further develop into affective disorders[10], hyper-vigilance[11] and overall decreased quality of life. This model is consistent with the plethora of data that stresses the importance of patients accepting that pain relief is unachievable in clinical treatment of chronic pain[12],[13].

2. Effects of pain on higher cognitive processes

2.1 Attentional interruption

Attentional selection is the cognitive process of filtering the overload of sensory input down to useful and relevant information. This process can occur in a top-down or a bottom-up method. The top-down attentional selection is the process of selection of a set of stimuli that are relevant to the cognitive goals activated in the working memory. This is achieved by increasing or decreasing the sensitivity of neurons responding to relevant or irrelevant stimuli respectively[14]. Bottom-up attentional selection is the capture of attention by the sensory stimuli themselves. This is often new or deviant sensory information that is more readily detected than stimuli for which a person is accustomed to[15].
Among the possible deviant stimuli recognized by the working memory in the bottom up manner, pain is one of them. Bottom up selection of nociception and top down selection of goal directions seems to compete for limited attentional resources. This is supported by the fact that pain disrupts executive processing of selective attention, attention span, attentional switching and divided attention[16],[17]. This model of pain and cognitive performance sharing resources is consistent with neuroimaging meta-analysis that found pain related activity in lateral and anterior prefrontal cortex (PFC) that are also strongly implicated in various executive processes[18],[19]. Other areas such as the Midcingulate cortex (MCC) and the operculo-insularareas have been suggested to be important in orientation of attention to salient and painful stimuli[20],[21].

2.2 Hyper-vigilance

Although pain generally orients an individual’s immediate attention to pain and possible routes for analgesia, some individuals also show greatly increased vigilance for pain. Individuals become more vigilant to the hurt area to determine its status and confirm whether any attempts at analgesia has succeeded. Although this is a normal response to pain, it is not uncommon for individuals with constant or recurrent pain experiences to develop a habit of hyper-vigilance, where they are constantly worrying too much about their pain. This state of increased attentional dedication to pain has been suggested to be linked to dominant anxiety and poor concentration observed in certain chronic pain conditions[2]. Hyper-vigilance then can mediate a top-down response to increase pain intensities as reported by patients. Individuals with hyper-vigilance also show increased use of health-care resources and increased emotional distress[22].

2.3 Depression

Repeated or prolonged exposure to nociceptive experience in chronic pain seems to cause distinct cognitive changes resulting in depression. It is hypothesized that during chronic pain, the schemas for pain, illness and the self begin to intersect to cause association of negative affect with self-identification inducing depression. A schema is a stored body of knowledge whose contents are interconnected and serve to facilitate data retrieval. When an element in a schema is activated, there is a preferential activation of elements close to it in the schema. During chronic pain, the patients’ schemas for pain, illness and the self begin to intersect or enmesh, and events that used to activate elements with benign consequences can activate a cascade of negative elements that are now connected by schema enmeshment. The resulting negative bias in self-identification to cause depression[23]. This theory is consistent with the fact that individuals who became depressed due to chronic pain were found to report more negative health related responses in a sentence completion task[24] as well as bias in memory with deteriorated recall of positive words[25]. Furthermore, perceived impact from and perceived control of chronic pain seem to be significant predictors of depression in addition to pain intensity[26].

3. Mediation of pain by higher cognitive processes

3.1 Placebo & Nocebo

placebo analgesia is when a non-analgesic substance or procedure evokes reduction in pain sensation. The reverse phenomenon is the nocebo hyperalgesia, when there is a lack of recovery or worsening of condition despite administration of a known analgesic or treatment. In the context of pain, positive and negative suggestion accompanying sham or real treatment has been shown to modulate an individual’s nociceptive experience[27]. This modulation of pain experience was shown not to be a simple bias in pain reporting but complex response including physiological modulation of nociceptive signaling in the central nervous system (CNS).

General model of the Placebo analgesia Effect
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Table summarizing the elements of the induction, mediation and effects of placebo analgesia.
Adapted from Manchikanti et al. 2011. [3] Originally from adapted and modified from Goffaux P et al. 2010 [37]

3.1.1 Neurophysiological Mechanism

Neurophysiological Mechanism of Placebo Analgesia and Nocebo Hyperalgesia
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Placebo and nocebo effects on pain modulate central nervous system pain signaling
through 2 distinct pathways; one that is endogenous opioid mediated and the other CCK mediated.
Adapted from Manchikanti et al. 2011. [3] Originally from adapted and modified from Goffaux P et al. 2010 [37]
based on Colloca and Benedetti 2005 [38]

Placebos and the associated expected analgesia cause an activation of anterior cingulate cortex (ACC) to cause endogenous opioid activity in the periaqueductal gray (PAG) cell bodies. These PAG cell bodies project as a descending inhibitory pathway to the spinal cord which reduces the intensity of the afferent nociceptive signaling. This consequently decreases the amount of pain experienced by the individual[28],[29].

Nocebos and the associated suggestion of hyperalgesia cause anxiety which in turn activates cholecystokinin (CCK), a neurohormone in the CNS. CCK is most likely the key signaling hormone for nocebo hyperalgesia as administration of glumide, a CCK-receptor antagonist blocks expectation induced hyperalgesia[30]. CCK directly activates “ON” cells which in turn activates pronociceptive efferent circuits of rostroventral medulla and the excitatory bulbospinal circuits to increase pain signaling intensity in the spinal cord[31],[32]. CCK may also activate the spine directly based on CCK receptors showing similar distribution patterns as opioid receptors involved in placebo analgesia[33]. Although CCK is induced by anxiety, it has been shown that CCK also induces anxiety response through adrenocorticotropic hormone and cortisol increase. However this pathway seems to be independent of the pain hyperalgesia pathway[34]

3.1.2 Clinical importance

The placebo effect is commonly discussed in studies that evaluate treatments as it does make it more difficult to prove their efficacy. This can be especially problematic because new treatments are more likely to elicit a placebo response than an existing treatment. Consequently clinical trials of new treatments involve a double blind study with placebo controls, designed so that neither the patients nor the researchers are aware whether patients are receiving the active or placebo treatment[35]. This has been shown to greatly reduce placebo effect since patients do not have strong expectations[36].
While its place in clinical trials of new treatments have associated placebo effects with negative connotations of ‘sham’ treatments and ‘false effects’, it is an important effect to capitalize on in the clinical setting when treating actual patients with pain. Providing a reassuring environment with positive expectations can induce a placebo effect to increase the efficacy of the current treatment, thereby decreasing the need to resort to more potent, but often more side-effect prone treatments. It is also important to be mindful of the nocebo effect, as the decreased efficacy of treatment resulting from a negative environment can prevent the success of a treatment that otherwise would have been effective. The use of expectation to increase or block effects of genuine analgesics has previously been shown[29]. Ideally, the physician should work with the patient to create realistic but positive expectations through confidence in treatment that will not cause disappointment in the patient even if it fails. Disappointment through exaggerated and false expectations could cause patients to become much more negative and catastrophic for future treatments and decrease their efficacy. The current practice of analgesic administration is to begin with small doses of analgesic then increase the doses as successive treatments fail. This practice has been questioned to increase the likelihood of subsequent treatment failures due to the initial inefficacy causing negative expectations and consequently the nocebo hyperalgesia in the patient[3]

1. Eccleston, C. (2013). A normal psychology of everyday pain. International Journal of Clinical Practice, 67, 47-50. doi:10.1111/ijcp.12051
2. Eccleston, C. (2001). Role of psychology in pain management. British Journal of Anaesthesia, 87(1), 144-152.
3. Manchikanti, L., Giordano, J., Fellows, B., & Hirsch, J.A. (2011). Placebo and Nocebo in interventional pain management: A friend or a foe – or simply foes? Pain Physician, 14, E157-175.
4. Bush, G., Luu, P., & Posner, M.I. (2000). Cognitive and emotional influences in anterior cingulate cortex. Trends in Cognitive Sciences, 4(6), 215-222.
5. Meerwijk, E.L., Ford, J.M., & Weiss, S.J. (2013) Brain regions associated with psychological pain: implications for a neural network and its relationship to physical pain. Brain Imaging and Behavior, 7, 1-14. doi:10.1007/s11682-012-9179-y
6. Meir, L., Strand, L.I., & Alice, K. (2012). A model for pain behavior in individuals with intellectual and developmental disabilities. Research in Developmental Disabilities, 33, 1984-1989, doi:10.1016/j/ridd.2012.05.028
7. Lotan, M., Moe-Nilssen, R., Ljunggren, A.E., & Strand, L.I. (2009). Measurement properties of the Non-Communicating Adult Pain Checklist (NCAPC): A pain scale for adults with Intellectual and Developmental Disabilities, scored in a clinical setting. Research in Developmental Disabilities, 31, 367-375. doi:10.1016/j.ridd.2009.10.008
8. Walkenhorst, E., & Crowe, S.F. (2009) The effect of state worry and trait anxiety on working memory processes in a normal sample. Anxiety, Stress, & Coping: An International Journal, 22(2), 167-187, doi: 10.1080/10615800801998914
9. Eccleston, C., & Crombez, G. (2007). Worry and chronic pain: A misdirected problem solving model. Pain, 132, 233-236. doi:10.1016/j.pain.2007.09.014
10. Niles, A.N., Lebeau, R.T., Liao, B., Glenn, D.E., & Craske, M.G. (2012). Dimensional indicators of generalized anxiety disorder severity for DSM-V. Journal of Anxiety Disorders, 26, 279-286. doi:10.1016/j.janxdis.2011.12.007
11. Crombez, G., Damme, S.V., & Eccleston, C. (2005). Hypervigilance to pain: An experimental and clinical analysis. Pain, 116, 4-7. doi:10.1016/j.pain.2005.03.035
12. McCracken, L.M., Carson, J.W., Eccleston, C., & Keefe, F.J. (2004). Acceptance and change in the context of chronic pain. Pain, 109, 4-7. doi:10.1016/j.pain.2004.02.006
13. Vowles, K.E., Witkiewitz, K., Sowden, G., & Ashworth, J. (2014). Acceptance and Commitment Therapy for Chronic Pain: Evidence of Mediation and Clinically Significant Change Following an Abbreviated Interdisciplinary Program of Rehabilitation. Journal of Pain, 15(1), 101-113. doi:10.1016/j.jpain.2013.10.002
14. Desimone, R. & Duncan, J. (1995). NEURAL MECHANISMS OF SELECTIVE VISUAL ATTENTION. Annual Reviews Neuroscience, 18, 193-222.
15. Ayala, Y.A., & Malmierca, M.S. (2013). Stimulus-specific adaptation and deviance detection in the inferior colliculus. Frontiers in Neural Circuits, 6, Article 89 doi: 10.3389/fncir.2012.00089
16. Moore, D.J., Keogh, E., & Eccleston, C. (2013). The effect of threat on attentional interruption by pain. Pain 154, 82–88. doi:10.1016/j.pain.2012.09.009
17. Keogh, E., Cavill, R., Moore, D.J., Eccleston, C. (2014). The effects of menstrual-related pain on attentional interference. Pain, 155, 821-827. doi:10.1016/j.pain.2014.01.021
18. Peyron, R., Laurent, B., & Garcia-Larrea, L. (2000). Functional imaging of brain responses to pain. A review and meta-analysis. Clinical Neurophysiology, 30, 263-288.
19. Wager, T.R., & Smith, E.E. (2003). Neuroimaging studies of working memory: A meta-analysis. Cognitive, Affective, & Behavioral Neuroscience, 3(4), 255-274.
20. Downar, J., Mikulis, D.J., David, K.D. (2003). Neural correlates of the prolonged salience of painful stimulation. Neuroimage, 20, 1540-1551. doi:10.1016/S1053-8119(03)00407-5
21. Legrain, V., Perchet, C., & Garcia-Larrea, L. (2009). Involuntary orientation of attention to pain and behavioural distraction. A study with laser and visual evoked potentials. Journal of Neurophysiology, 102, 2423-2434. doi:10.1152/jn.00372.2009
22. McCracken, L.M. (1997). “Attention” to Pain in Person With Chronic Pain: A Behavioral Approach. Behavior Therapy, 28, 271-284.
23. Pincus, T., & Morley, S. (2001). Cognitive-Processing Bais in Chronic Pain: A Review and Integration. Psychological Bulletin, 127(5), 599-617. doi: 10.1037/0033-2909.127.5.599
24. Rusu, A.C., Pincus, T., & Morley, S. (2012). Depressed pain patients differ from other depressed groups: Examination of cognitive content in a sentence completion task. Pain, 153, 1898-1904. doi:10.1016/j.pain.2012.05.034
25. Pauli, P., & Alpers, G.W. (2002). Memory bias in patients with hypochondriasis and somatoform pain disorder. Journal of Psychosomatic Research, 52, 45-53.
26. Turk, D.C., Okifuji, A., & Scharff, L. (1995). Chronic pain and depression: role of perceived impact and perceived control in different age cohorts. Pain, 61, 93-101.
27. Manchikanti, L., Pampati, V., & Damron, K. (2005). The Role of Placebo and Nocebo Effects of Perioperative Administration of Sedatives and Opioids in Interventional Pain Management. Pain Physician, 8, 349-355.
28. Wager, D. (2004). Placebo-Induced Changes in fMRI in the Anticipation and Experience of Pain. Science, 303, 1162-1167. doi:10.1126/science.1093065
29. Goffaux, P., Redmond, W.J., Rainville, P., & Marchand, S. (2007). Descending analgesia – When the spine echoes what the brain expects. Pain, 130, 137-143. doi:10.1016/j.pain.2006.11.011
30. Benedetti, F., Amanzio, M., Casadio, C., Oliaro, A., & Maggi, G. (1997). Blockade of nocebo hyperalgesia by the cholecystokinin antagonist proglumide. Pain, 71(2), 135-140. doi:10.1016/S0304-3959(97)03346-0
31. Field, H. (2004). State-dependent opioid control of pain. Nature Reviews Neuroscience, 5, 565- 575. doi:10.1038/nrn1431
32. Heinricher, M.M., & Neubert, M.J. (2004). Neural Basis for the Hyperalgesic Action of Cholecystokinin in the Rostral Ventromedial Medulla. Journal of Neurophysiology, 92, 1982-1989. doi:10.1152/jn.00411.2004
33. Magnuson, D.S.K., Sullivan, A.F., Simmonet, G., Roquest, B.P., & Dickenson, A.H. (1990). Differential Interactions of Cholecystokinin and FLFQPQRF-NH2 with μ and δ Opioid
Antinociception in the Rat Spinal Cord. Neuropeptides, 16, 213-218.
34. Benedetti, F., Amanzio, M., Vighetti, S., & Asteggiano, G. (2006). The Biochemical and Neuroendocrine Bases of the Hyperalgesic Nocebo Effect. Journal of Neuroscience, 26(46), 12014-12022. DOI:10.1523/JNEUROSCI.2947-06.2006
35. Finniss, D.G., & Benedetti, F. (2005). Mechanisms of the placebo response and their impact on clinical trials and clinical practice. Pain, 114, 3-6. doi:10.1016/j.pain.2004.12.012
36. Vase, L., Riley, J.L., & Price, D.D. (2002). A comparison of placebo effects in clinical analgesic trials versus studies of placebo analgesia. Pain, 99, 443-452.
37. Goffaux, P., Léonard, G., Marchand, S., & Rainville, P. (2010). Placebo analgesia. In Beaulieu, P., Lussier, D., Porreca, F., Dickenson, A.H. (Eds), Pharmacology of Pain (451-473). Seattle: IASP Press.
38. Colloca, L., & Benedetti, F. (2005). Placebos and painkillers: is mind as real as matter? Nature Reviews Neurosciece, 6, 545-552

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