How Pain Cognitions Can Influence the Pain Experience

The following was written as a research paper to meet my massage therapy program’s writing requirements. As such, it is written for an academic audience in APA format and it may be dry and/or difficult reading for the general public. If this subject interests you, I’d advise first reading my article A Primer on Pain where I touch on many similar issues in an easier to read format. I never had any intent of posting this online, but many of my colleagues have encouraged me to do so. If you don’t like it, you have my full permission to blame them.

With very few exceptions, pain is a part of the human experience. Yet due to the complexity of pain, it is still an often poorly understood subject, even by those who treat it. This is especially important because what people believe about the nature of pain can greatly influence their pain experiences for better or for worse.

To best understand why pain cognitions matter, it is important to first understand what pain is and is not. However, discussing the modern scientific understanding of pain without examining the history of pain theory fails to address many of the inaccurate and potentially harmful beliefs that remain pervasive today. By exploring the conclusions of modern pain science in the context of the history of pain theory, a much greater understanding of pain can be had.

Up until the latter half of the 20th century, pain was largely understood through the lens of Specificity Theory. Created by 17th century philosopher Rene Descartes, Specificity Theory states that physical harm to the person activates specific peripheral pain sensing nerve fibers, which send messages up the spinal cord and into the pain center of the brain where pain is then experienced. In this view, pain always has a direct physical cause and the amount of pain a person feels has linear relationship to the severity of their injury. This narrow understanding left patients with no clear etiology without any help, and frequently labeled as mentally disturbed or damaged (Melzack & Katz, 2013 p.2).

The next major step forward in pain theory was the introduction of the Gate Control Theory by Ronald Melzack and Patrick Wall in 1965. Melzack and Wall suggested that pain is felt when activation of peripheral nerve fiber signals reach a certain threshold in the dorsal horn of the spinal cord. Once this threshold is met, action signals are sent to the brain where they are interpreted and pain is then experienced. The Gate Control Theory also described the brain’s ability to increase or decrease the demands of the activation threshold required for the brain to receive the signals involved in pain. This allowed for inclusion of contextual and psychological factors in the pain experience, thus allowing for a wide variety of treatments including multidisciplinary treatments for those who had previously been labeled psychologically damaged (Melzack & Katz, 2013 p.2-3).

While the Gate Control Theory proved to add much both clinically and intellectually, it still could not account for the pain experienced by numerous patients. Particularly of note were those with phantom pain. Paraplegic patients without sections of their spinal cord could still experience pain below the level of their missing spinal cord, which should have proved impossible if the Gate Control Theory offered a complete picture (Melzack & Katz, 2013 p.3-4).

The continued study of phantom limb and phantom body patients throughout the years offered a number of different insights not only on the nature of pain, but on how we as humans construct and experience our bodies and ourselves. Melzack and Katz (2013) explain:

First, because the phantom limb feels so real, it is reasonable to conclude that the body we normally feel is subserved by the same neural processes in the brain as the phantom; these brain processes are normally activated and modulated by inputs from the body but they can act in the absence of any inputs. Second, all the qualities of experience we normally feel from the body, including pain, are also felt in the absence of inputs from the body; from this we may conclude that the origins of the patterns of experience lie in neural networks in the brain; stimuli may trigger the patterns but do not produce them. Third, the body is perceived as a unity and is identified as the ‘self’, distinct from other people and the surrounding world. The experience of a unity of such diverse feelings, including the self as the point of orientation in the surrounding environment, is produced by central neural processes and cannot derive from the peripheral nervous system or spinal cord. Fourth, the brain processes that underlie the body-self are ‘built- in’ by genetic specification, although this built-in substrate must, of course, be modified by experience, including social learning and cultural influences. (p. 4)

The revelation that physical experiences including pain could be created in the brain without input from the peripheral system necessitated a new explanatory model. This model, put forth by Ronald Melzack in 1999 is known as The Neuromatrix Theory. (Melzack & Katz, 2013 p.4).

The Neuromatrix Theory suggests that the perception of the physical self is a flexible interconnected emergent neural output that is modulated (rather than caused) by peripheral input. While heat and injury exist as physical events, they are distinctly different and must be separated from the experience of warmth and pain (Melzack & Katz, 2013 p.4-5). Pain can exist without an identifiable physical cause and conversely, postural, structural, and biomechanical indicators of dysfunction or damage can be found in abundance in completely asymptomatic populations (Lederman, 2011 p.131-132). Moseley (2007) also notes that “The relationship between pain and the state of the tissues becomes weaker as pain persists” (p.171). This understanding offers great challenges to the previous models and accurately informs the current modern scientific perspectives on pain.

Due to the complex and multi-factorial understanding of the nature of pain, it is very difficult to provide a definition of pain that reflects a complete understanding of the subject. Despite this challenge, many great minds have tried. Cohen, Quintner, and Buchanan (2013) observe:

The generally accepted definition of pain, as adopted in 1979 by the International Association for the Study of Pain (IASP), is “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (p.1).

Moseley (2007) prefers to say “…that pain can be conceptualised as a conscious correlate of the implicit perception that tissue is in danger.” (p.169). The strengths in both of these definitions are the acknowledgments that pain can be present with or without any musculoskeletal dysfunction or danger, and that pain is the response to a perceived threat.

The recognition of pain as an experience in reaction to perceived threat has had tremendous implications. Moseley (2007) explains “Fundamental to the paradigm is that anything that modulates implicitly perceived threat should be relevant. That means that psychosocial factors, including anxiety, depression, attitudes and beliefs, social context or work status may all play an important role.” (p.175). Perceptions are flexible and modifiable based on a near limitless variety of factors, therefore pain can never have a clearly identified cause, but many of the relevant influencing factors can be addressed.

Perhaps one of the most striking examples of the influence of beliefs on pain is the story of a builder who arrived in the emergency room in severe pain. Dimsdale and Dantzer (2007) recount the event:

In one report, Fisher et al. described the case of a builder who jumped down onto a 7-inch nail, which pierced his boot at the toe level. The man was in pain and required intravenous sedation in the emergency room. However, when the boot was cut away, it turned out that the nail had fortunately passed between his toes as opposed to its apparent impaling of the foot. The man’s agonizing pain was elicited solely by his misperception—a case of somatic amplification. (p.3).

While a rather extreme (and likely rare) example, this case clearly demonstrates that the presence of sufficiently convincing beliefs of harm can be a major contributing factor in the personal pain experience.

In their 2013 study on nocebo hyperalgesia, Stephan Geuter and Christian Büchel sought to examine how context and expectations can biologically and experientially impact pain. On the first day of this two day study, subjects had five different divisions marked on the palmar surface of the skin of their forearms. Each of these divisions except for the baseline had the same completely inert cream applied, but the context and information given upon application was different based on the application sites. For two of the divisions, cream was dispensed from a container labeled with a name suggesting its harmless nature, and subjects were correctly informed that the inert cream would have no negative influence on their pain experience. For another two divisions, cream was applied from a container that suggested the contents contained capsaicin, which was explained to increase local pain sensitivity. The final division had no application and was used as a baseline for calibration purposes (Geuter & Büchel, 2013 p.13785).

Following the application and explanation of the cream, baselines were taken for pain thresholds and pain ratings in response to a variety of different heat stimuli applied to the arm via a heat thermode device. This procedure allowed for the attribution of numerical values to the subjects’ intensity of pain. Geuter and Büchel (2013) explain the implementation of manipulating subject expectations:

After the calibration series, subjects completed a demographic questionnaire, the Pain Catastrophizing Scale (PCS), and the Social Desirability Scale (SDS). Following the questionnaires, a first manipulation session was conducted. Subjects received six heat stimuli on the control and nocebo patches, respectively. The stimulation order was counterbalanced across subjects. The temperature on the control patch was calibrated to elicit a pain rating of 40, whereas the temperature on the nocebo patch was calibrated to elicit a pain rating of 80. Critically, subjects were led to believe that the temperatures were equal and that all differences in pain were due to the “capsaicin cream.” (p.13785)

Following this pain exposure, a pain rating questionnaire was administered to the subjects and the first day’s session concluded.

The second day of the study began with subjects undergoing very similar contextual manipulation as performed on the first day. Patches of skin on the forearms were divided into five sections, with two knowingly inert sections, one baseline division, and two nocebo sections. Once again a heat thermode (falsely) stated to be the same temperature for each exposure was applied to the skin to create the experience of greater pain intensity at the site of nocebo application. The only difference between contextual manipulation on the first and second days was that manipulation occurred inside an fMRI scanner which was not recording data at the time (Geuter & Büchel, 2013 p.13786).

Following a series of breaks and further evaluations, subjects returned to the fMRI scanner for continued experimentation. Geuter & Büchel (2013) describe the protocol:

After returning to the scanner, subjects received 15 heat stimuli in each condition, rating their experienced pain after each stimulus. The temperature was now set to a VAS of 60 and was identical in both conditions. During the test session, we recorded fMRI data of the spinal cord (see Data acquisition), as well as respiration rate and heart rate to correct for physiological noise in the fMRI data (Brooks et al., 2008; Kong et al., 2012). Finally, subjects left the MRI scanner, completed the questionnaire regarding experienced pain a second time, and were debriefed. (p.13786)

The resulting data from subject surveys when combined with fMRI readings demonstrates the role of context and expectation in both biological and experiential terms.

When heat stimulus was applied to divisions on subjects’ forearms that had received nocebo manipulation there was a significantly increased pain rating when compared to the knowingly inert control. Additionally, subjects demonstrated lower pain thresholds with nocebo treated patches when compared to control (Geuter & Büchel, 2013 p.13787). With regard to subjective measures, Geuter and Büchel state “Hence, subjects experienced lower temperatures as painful and perceived identical stimuli as more painful following nocebo treatment.” (p.13787)

The results from fMRI imaging offer a possible biological contribution in the explanation for the changes in subjective pain measures. Changes in the threat signal processing areas of the spinal cord reveal increased activity in areas that corresponded to the where subjects’ forearms were treated with nocebo when compared to control. This suggests that context and expectations can create pre-cortical physical changes in the processing of threat signals (Geuter & Büchel, 2013 p.13787). Geuter and Büchel (2013) conclude:

In summary, the observed nocebo amplification of spinal pain signals demonstrates a cognitive facilitation of pain processing in humans at the first relay of incoming nociceptive signals. When expectations increase pain signals before cortical processing, the subjective pain experience may rely on exaggerated pain information, making it harder to ignore the pain. People, who constantly expect some action to be painful, will experience this action as more painful due to increased pain signals. This in turn, will strengthen the pain-enhancing expectations. In case such pain-exaggerating thoughts are maintained over a long time, these may eventually support the chronification of pain (p. 13789)

This study demonstrates the role of negative expectations and context on the pain experience, and further provides a plausible mechanism by which tolerance to noxious stimuli of peripheral origin are lowered, and threat signals are amplified.

Researchers have found a unique population in Aboriginal Australians that demonstrates the influence of pain cognitions that is consistent with theories of modern pain science. Aboriginal Australians as a whole have historically suffered from a very low incidence of disabling chronic low back pain (CLBP) when compared to Western societies. A large part of the suspected reason for this finding is the influence of cultural beliefs about the nature of low back pain. Traditional Aboriginal Australian beliefs recognize CLBP as a temporary natural part of life that is likely to improve. This suggests that a lesser presence of negative pain cognitions and greater prevalence of positive expectations are associated with less disabling CLBP. (Lin et al., 2013 p.2) Given the possibly protective nature of traditional Aboriginal Australian beliefs to disabling chronic low back pain, examining the beliefs of those within this population who were disabled by their CLBP proves to be especially insightful.

Within this population, Lin et al. (2013) note that, “More than half of the participants believed that there were one or more structural or anatomical problems of their spine that were responsible for the cause of their pain” (p.4). With few exceptions, those who believed their CLBP to be caused by postural, structural, or biomechanical factors had high to moderate levels of disabling pain, a more negative outlook, and less hope for future outcomes. (Lin et al., 2013 p.4-5)

Conversely, those who were demonstrated uncertainty in the cause of their pain experienced mild disabling pain. Additionally, these participants were more likely to believe their pain could be managed with self-care, and they also held positive beliefs about future outcomes (Lin et al, 2013 p.6)

This understanding is consistent with research done on how language influences emotional state, which has been tied to pain and disability outcomes. As a trend, language that stated or implied damage or dysfunction provoked a more negative emotional state (Vranceanu et al., 2011 p.114).

It is entirely plausible that the belief in physical harm or defect as the cause of pain creates a bleak narrative where one feels broken and hopeless, which increases pain and disability. This is why numerous trials aimed at correcting these inaccurate and harmful beliefs using Neuroscience Education (NE) have been done. Louw, Diener, Butler, and Puentedura (2011) explain that:

NE can be best described as an educational session or sessions describing the neurobiology and neurophysiology of pain, and pain processing by the nervous system. Instead of a traditional model of connecting tissue injury or nociception and pain, NE aims to describe how the nervous system, through peripheral nerve sensitization, central sensitization, synaptic activity, and brain processing, interprets information from the tissues and that neural activation, as either upregulation or downregulation, has the ability to modulate the pain experience. (p.2041-2042)

The goal of NE is to reduce patients’ fear, anxiety, and pain through understanding pain as an output of the nervous system in response to a perceived threat rather than as an indicator of tissue health. This promotes movement and self-efficacy, and may reduce the chances of pain becoming chronic. (Louw et al., 2011 p.2042)

To evaluate the efficacy of neuroscience education, Louw et al. (2011) performed a systematic literature review of NE using primarily randomized control trials (p.2044). Upon review, it was noted that there were a number of differences between these trials. NE was frequently used alongside other interventions including a variety of different forms of manual therapy and/or exercise protocols that varied by study. Additionally, there were variations in the duration, frequency, and format for the delivery for NE. However, all patients involved in these studies were suffering from chronic pain, and almost every trial included NE delivered to patients verbally by physical therapists. (Louw et al., 2011 p.2044-2050). Louw et al. (2011) acknowledge these differences, but conclude:

Although this review comprised a rather heterogeneous sample of studies using NE, the results indicate compelling evidence for the use of NE in decreasing pain ratings, increasing physical performance, decreasing perceived disability, and decreasing catastrophization in patients with chronic MSK pain. (p.2052)

From this review, it is safe to say that accurate and positive beliefs about pain improve a variety of clinically meaningful outcomes in those experiencing chronic pain.

While most studies on the effects of pain cognitions to date have been performed in chronic pain patient populations, there has also been some limited research on how an accurate understanding of pain can reduce future incidence of pain. In a large scale two year military study evaluating low back pain, soldiers were divided into four different groups, which each performed a series of supervised exercises for an equal duration of time. Two of these groups performed a traditional exercise program (TEP) whereas the other two groups performed a core stabilization exercise program (CSEP). One group from each the TEP and the CSEP were then selected to undergo a 45 minute lecture about the nature of low back pain and were also provided a short book that provided similar information. (George et al., 2011 p. 2-3)

Results from this study demonstrate that regardless of the exercise program used, soldiers who received pain education sought medical care for low back pain significantly less than the other groups (George et al., 2011 p. 5-6). Because low back pain outcomes were evaluated via the number of soldiers who received medical care, it is difficult to know how pain experiences between groups differed qualitatively (George et al., 2011 p. 7-8). It is possible that soldiers who received pain education had superior pain coping strategies, which made them more confident in delaying or foregoing medical care. While self-efficacy and positive outlook are closely linked to the successful resolution of pain, this confounding factor makes it difficult for this study provide an entirely accurate reflection of the incidence of pain among soldiers in this study. However, in light of the greater body of research regarding the influence of context and beliefs on the pain experience, there are plausible mechanisms that suggest pain intensity and duration may have been reduced in those who received pain education.

When evaluating the evidence on the whole, it is very clear that what people believe about the nature of pain can positively or negatively influence their pain experience. Beliefs that promote a direct cause of pain from damage or dysfunction are not only inaccurate, but can also do harm to the people who hold them. Louw et al. (2011) clearly state:

Orthopedic-based professions such as orthopedic surgeons and physical therapists commonly use anatomy- and pathoanatomy-based models to explain pain to their patients.Not only have these models shown limited efficacy in decreasing pain and disability, but they may increase fear in patients, which in turn, may increase their pain (p.2052)

Yet beliefs that accurately represent the modern scientific understanding of pain can decrease pain intensity, increase pain thresholds, and possibly even reduce the incidence of future pain. For these reasons it is of the utmost importance that those who suffer from and are involved in the treatment of pain learn to understand its true nature.

 

References

Cohen M., Quintner J., & Buchanan D. (2013).Is chronic pain a disease?
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Dimsdale JE, & Dantzer R. (2007). A biological substrate for somatoform disorders: importance of pathophysiology
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George SZ., Childs JD., TeyhenDS., Wu SS., Wright AC., Dugan JL., & Robinson ME. (2011). Brief psychosocial education, not core stabilization, reduced incidence of low back pain: results from the Prevention of Low Back Pain in the Military (POLM) cluster randomized trial
Biomed Central Medicine, 9:128 doi:10.1186/1741-7015-9-128

Geuter S, & Büchel C. (2013). Facilitation of pain in the human spinal cord by nocebo treatment.

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Lederman E. (2011). The fall of the postural-structural-biomechanical model in manual and physical therapies: exemplified by lower back pain.

Journal of Bodywork and Movement Therapies, 15(2):131-8. doi:10.1016/j.jbmt.2011.01.011.

Lin IB., O’Sullivan PB., Coffin JA., Mak DB., Toussaint S., & Straker LM. (2013). Disabling chronic low back pain as an iatrogenic disorder: a qualitative study in Aboriginal Australians.

BMJ Open. doi:10.1136/bmjopen-2013-002654

Louw A., Diener I., Butler DS., Puentedura EJ. (2011). The effect of neuroscience education on pain, disability, anxiety, and stress in chronic musculoskeletal pain.
Archives of Physical Medicine and Rehabilitation. 92(12):2041-56. doi:10.1016/j.apmr.2011.07.198.

Melzack, R., & Katz, J. (2013). Pain.

WIREs Cognitive Science, 4: 1–15. doi:10.1002/wcs.1201

Moseley, G. Lorimer. (2007). Reconceptualising pain according to modern pain science
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Vranceanu AM., Elbon M., & Ring D. (2011). The emotive impact of orthopedic words.

Journal of Hand Therapy. ;24(2):112-6; quiz 117. doi:10.1016/j.jht.2010.10.010

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