Pain is a complex, perceptual experience, defined as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”¹ One of the critical developments in the past several decades in pain research is the progress in our understanding of the multifactorial, biobehavioral mechanisms involved with chronic pain.² Research has consistently shown the importance of using multimodal approaches to treat patients with chronic pain³ because monotherapies appear to provide less than optimal relief.⁴ These developments have pointed to various psychological factors—cognitive, emotional, and behavioral—as significant contributors for pain modulation and pain-related disability.⁵

The main objective of this chapter is to review the various psychological factors relevant to the experience of pain. As a background, it is important to consider how we conceptualize pain. Our view of pain will influence our evaluations of patients who report pain and the nature of the interventions that we use to treat them. The way we conceptualize pain depends largely on the nature of the information acquired and the models that we were exposed to during our training. In the first section of this chapter, we review the historical models of how we conceptualized pain. We will argue that although these models are not necessarily inaccurate, they are incomplete. We then suggest that a broader, multidimensional perspective is required to understand pain and to treat patients appropriately. We describe the role of behavioral, cognitive, and affective factors that have been shown to be relevant to the experience of pain, disability, and response to treatment. We provide data demonstrating that these psychological factors may have an effect both on patients’ behavior and physiology. Finally, we raise the issue of the “patient uniformity myth” and describe the subgroups of pain patients based on psychosocial and behavioral characteristics. We provide data suggesting that knowledge of such patient subgroups may serve as a basis for matching patients to treatments based on their characteristics.

Historically, pain has been understood from the perspective of Cartesian dualism in which pain was viewed as purely sensory, reflecting the degrees of incoming noxious sensory stimuli. This perspective assumes that there are two ends to a pain pathway. At the periphery, there are sensory receptors (nociceptors), where noxious information is received and, at the other end, regions located in the brain where information is registered passively. From this perspective, noxious stimulation inevitably results in the sensation of pain, as if pulling a string at the periphery activates a bell located in the brain. Variations of this model have been prominent since first proposed by Descartes in 1644.

A central belief of sensory models is that the amount of pain experienced is a direct result of the amount, degree, or nature of sensory input or physical damage and is explained in terms of specific neuro physiological mechanisms. Clinically, it is expected that the report of pain will be directly proportional to the amount of pathology. This model dictates that assessment should focus on identifying the cause of the pain. Once identified, treatment should involve removal of the cause or severing or blocking the specific pain pathways by surgical or pharmacological means.

Sensory models continued to maintain a prominent position in medicine despite this model’s inability to account for a number of observations. For example,

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  Patients with equivalent degrees and types of objectively-determined tissue pathology vary widely in their reports of pain severity.

  
  
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  Patients with only minimal, objectively determined pathology may report severe pain.

  
  
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  Asymptomatic individuals often reveal significant amounts of physical pathology on imaging.

  
  
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  Procedures that might be expected to produce pain sometimes do not. For example, surgical procedures designed to inhibit pain transmission by severing neurological pathways believed to be underlying the reported pain may fail to alleviate pain.

  
  
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  Patients with equivalent degrees of tissue pathology who are treated with identical treatments respond in widely differently ways.

  
  
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  There are only modest associations among impairment, pain, and disability.

Thus, we see a number of paradoxes in clinical practice. There are patients who report severe pain with limited physical pathology and, conversely, patients who have significant physical pathology but no pain; pain pathways can be ablated but pain can persist; and identical treatments provided for the same diagnosis can result in different outcomes.

Unfortunately, for many with chronic pain, the underlying causes of pain frequently remain unknown, despite the development and use of sophisticated diagnostic imaging procedures such as CT (computed tomography) scan or MRI (magnetic resonance imaging). For example, objective evidence of physical pathology is only identified in about 15% of the cases of back pain.⁶ In knee osteoarthritis (OA), physical findings such as cartilage loss and bone marrow edema are considered to reflect the progression of the disease and clinical presentations. However, when the grading of pathology by the imaging (MRI) was evaluated, neither bone marrow edema nor cartilage abnormality were linearly related to pain severity.⁷ Similarly, an MRI study of a total of 256 hips has shown that the large number of hips with no pain showed various degrees of peritrochanteric MRI abnormalities, when compared to those hips with pain.⁸

How can such paradoxes be understood? As is frequently the case in medicine, when objective physical evidence and explanations prove inadequate to explain symptoms, psychological alternatives are proposed. If the pain reported by a patient is believed to be disproportionate to objectively determined physical pathology or if the complaint is recalcitrant to “appropriate” treatment, then it is assumed that psychological factors must be involved, even if not causal. Thus, there appears to be a somatogenic–psychogenic dichotomy in how the report of pain is construed.

It is important to realize that determination of whether the reported pain is disproportionate is subjective. There is no objective way to determine how much pain is proportionate to the underlying condition. How much should a given amount of tissue pathology hurt? Similarly, determination of appropriate treatment is not totally objective. Different health care providers might recommend widely different treatments for patients with the same presenting symptoms.⁴ For example, treatments for patients with temporomandibular disorders range from surgery to psychotherapy and, for fibromyalgia, from electroconvulsive therapy to sulfur mud baths.

The somatogenic–psychogenic dichotomy forms the basis for the distinction underlying attempts to identify “functional” versus “organic” pain, as well as references to a “functional overlay.” The American Psychiatric Association⁹ created two psychiatric diagnoses associated with pain in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders—pain associated with psychological factors either with or without a diagnosed medical condition. The specific diagnosis of “pain disorder associated with psychological factors and a general medical condition” is characterized by the fact that both psychological factors and a general medical condition have important roles in the onset, severity, exacerbation, and maintenance of pain. This set of diagnoses is so broadly defined, however, that virtually all patients who have persistent pain may be diagnosed as suffering from a psychiatric disorder.

A variation of the dichotomous somatic–psychogenic views is a conceptualization that may be ascribed to by many insurance companies and other third-party payers. They suggest that if physical pathology is insufficient to support the claim of pain, then the complaint is suspect. Pain is assumed to result from symptom exaggeration to achieve some benefit (e.g., prescription medication, avoidance of undesirable activity, attention) or outright malingering (i.e., financial compensation). The assumption is that reports of pain without adequate biomedical evidence are motivated primarily by desire for some type of reinforcement. This belief has resulted in a number of attempts to catch malingerers using surreptitious observational methods (e.g., surveillance, video recording) and the use of sophisticated biomechanical machines geared toward identifying inconsistencies in functional performance. There is, however, very little empirical support for this belief. No studies, for example, have demonstrated dramatic improvement in pain reports subsequent to receiving disability awards (i.e., no further need to exaggerate symptoms).

The conceptualizations described here view physical and psychological factors as if they are mutually exclusive. Before examining models that attempt to integrate psychological factors with somatic factors, let us examine the nature of the psychological processes and factors that have been demonstrated to play an important role in pain perception, disability, and response to treatment.

A number of psychological principles based in learning theory have been extended to pain. These principles provide helpful explanations for many clinical observations. Moreover, a number of cognitive and affective factors have been demonstrated to influence expressions of pain and participation in rehabilitation. We can consider the major psychological, sociocultural, and behavioral principles and factors studied and then consider how they can be integrated to create a comprehensive, integrated model of pain that can serve as a guide for assessment and ultimately treatment.

OPERANT LEARNING MECHANISMS

As long ago as the mid-20th century, the effects of environmental factors in shaping the experience of pain were acknowledged. A new era in thinking about pain began in 1976, when Fordyce¹⁰ extended the principles of “operant conditioning” to chronic pain and disability.

In the operant conditioning formulation, behavioral manifestations of pain rather than pain per se are central. When a person experiences a noxious sensation, the initial response is a withdrawal or escape response. This may be accomplished by avoidance of the activity believed to cause or exacerbate pain, seeking help to reduce symptoms, and so forth. These behaviors are observable and, consequently, subject to the principles of operant conditioning—namely, reinforcement and avoidance learning.

The operant view proposes that pain behaviors such as avoidance of activity to protect an injured body part from producing additional noxious input may come under the control of external contingencies of reinforcement (responses increase or decrease as a function of their reinforcing consequences). It is these reinforcement contingencies that contribute to the maintenance of the problems associated with chronic pain and disability. Pain behaviors (e.g., limping, grimacing, and inactivity) are conceptualized as overt expressions of pain, distress, and suffering. These behaviors may be positively reinforced directly, for example, by attention from family or health care providers. Pain behaviors may also be maintained by the escape from noxious stimulation provided by the use of drugs or rest or the avoidance of undesirable activities such as work. In addition “well behaviors” (e.g., activity, working) may not be positively reinforcing and the more rewarding pain behaviors may, therefore, be maintained.

In an experimental study,¹¹ healthy volunteers’ facial expressions in response to noxious stimulation could readily be operantly conditioned by a simple reinforcement method either toward a greater or lesser degree of behavioral exhibition. We can also illustrate the role of operant factors in a case of chronic back pain. When a woman with painful back has a flare up, she may lie down on the floor and hold her back. Her husband may notice these dramatic behaviors and infer that she is experiencing pain. The husband’s behavioral response is influenced by his observation of her behavior. He typically responds to her pain displays by spending extra time with her and massaging her back. In this case, the woman’s lying down has resulted in receiving attention from her significant other, a positive consequence. According to the laws of operant learning, behaviors resulting in a positive consequence increase their chances of recurring.

Another powerful way the husband might reinforce his wife’s pain behaviors is by permitting her to avoid undesirable activities. When observing his wife lying on the floor, the husband suggests that they cancel the evening plans with his brother. If the person experiencing pain would prefer not to spend time with her husband’s brother, then the avoidance of the undesirable activity is reinforced and may contribute to reports of pain whenever activities with her husband’s brother are planned. In this situation, her pain reports and other behaviors are rewarded both by her husband providing her with extra attention and support and the opportunity to avoid an undesirable social obligation.

Whether operantly conditioned pain behaviors contribute to worsening of pain is somewhat controversial. Based upon the “facial feedback hypothesis” that asserts that overt behaviors affect internal sensory-emotional experience,¹² we may expect that as people’s pain behaviors are reinforced, their pain complaints increase. Salomons and colleagues¹³ trained their subjects to pain-related and relaxed facial expression. Unpleasantness rating of the noxious heat stimulus was greater when they were told to make a “pain” face than a “relaxed” face, providing some support for the facial feedback theory. However, in this experiment, the facial expressions were not subjected to any reinforcement schedules. On the other hand, in the aforementioned study by Kunz and colleagues,¹¹ the reinforced facial expression did not increase pain rating. When operant reinforcement is directly applied to a pain task in which contingent stimulus levels change, however, the prolonged sensitization to the noxious heat stimulus was enhanced, with the proportion linearly related to the level of reinforcement.¹⁴

Operant conditioning seems to have a consistent impact on disability. Particularly, postural guarding may be instrumental in acute to chronic disability of injured workers.¹⁵ A systematic review¹⁶ indicates that operant-based physical therapy significantly improves pain-related disability in chronic back pain patients.

It is important to clarify that the operant learning does not require a person with pain’s intentional and conscious efforts to elicit a desirable outcome. It results from a gradual learning process that neither the individual nor others tends to recognize as it unfolds. It should not, however, be assumed that pain behaviors are synonymous with malingering. Malingering involves the consciously and purposeful faking of symptoms such as pain for some gain, usually financial. In the case of pain behaviors, there is no suggestion of conscious deception but rather the unintended performance of pain behaviors resulting from laws of learning based on environmental reinforcement contingencies. The pain behavior in response to initial injury may encounter reinforcing events, thereby determining probability of that behavior recurring in the future; but, once the behavior is learned, the presence of initial pain is no longer needed for that behavior to recur.

The operant conditioning formulation does not concern itself with the initial cause of pain. Rather, it considers pain an internal subjective experience that can only be indirectly assessed and may be maintained even after an initial physical basis of pain has resolved. Because of the consequences of specific behavioral responses, it is proposed that pain behaviors may persist long after the initial cause of the pain is resolved or greatly reduced. Thus, in one sense, the operant conditioning model can be viewed as analogous to the psychogenic models described earlier. That is, psychological factors are treated as secondary reactions to sensory stimulation, rather than directly involved in the perception of pain per se.

The operant view has generated what has proven to be an effective treatment for select samples of chronic pain patients.¹⁷ Treatment focuses on eliminating pain behaviors by withdrawal of attention and increasing “well behaviors” (e.g., activity) by positive reinforcement. Although operant factors undoubtedly play a role in the maintenance of disability, exclusive reliance on the operant conditioning model to explain the experience of pain may not be appropriate. It has been criticized for its exclusive focus on motor pain behaviors, failure to consider the emotional and cognitive aspects of pain, and failure to treat the subjective experience of pain.¹⁸

RESPONDENT LEARNING MECHANISMS

Factors contributing to chronicity that have previously been conceptualized in terms of operant learning may also be initiated and maintained by classical or “respondent conditioning.”¹⁹ If an aversive stimulus is paired with a neutral stimulus for a number of times, the neutral stimulus will come to elicit aversive experiences in the individual. The patient learns to anticipate negative consequences even in the absence of the noxious stimulus. This process has been frequently observed in cancer patients receiving chemotherapy. Patients have been observed to report nausea when they enter the room where they have received the chemotherapy even before any cytotoxic medication has been administered. Similarly, a back pain patient who received a painful treatment from a physical therapist may become conditioned to experience a negative emotional response to the presence of the physical therapist, to a treatment room, and to any stimulus associated with the nociceptive stimulus (e.g., exercise equipment). The negative emotional reaction may lead to tensing of muscles, and this, in turn, may exacerbate pain, thereby reinforcing the association between the presence of the physical therapist and pain.

Probably, the most relevant emotional conditioning in pain is anxiety. Anxiety is often the affect underlying avoidance of activities. Pain patients often experience temporary aggravation of pain following physical activities. Avoiding such activities leads to no pain exacerbation, thus reinforcing inactivity and maintaining anxiety for activity. In other words, continuing to avoid specific activities will reduce disconfirmations that could provide corrective feedback.²⁰ Insofar as avoidance does not produce disconfirmation, the behaviors will persist.²¹ By contrast, when an anticipated consequence does not occur (disconfirmation), modification of learning also takes place. Thus, the physical therapist may have to encourage the patient to exercise to provide disconfirmation that, just because exercise may hurt, it will not automatically lead to increased injury. The therapist will have to emphasize that hurt and harm are not eqivalent. Both respondent conditioning and operant learning may contribute to the development and maintenance of dysfunctional behavioral patterns in chronic pain patients. Over time, more and more activities, people, and physical locations may be seen as eliciting or exacerbating pain and may be avoided (stimulus generalization). Fear of pain and avoidance may become conditioned to an expanding number of situations (response generalization). In addition to avoidance learning, pain may be exacerbated and maintained in these encounters with potentially pain-increasing situations because of the anxiety-related sympathetic activation and muscle tension increases that may occur in anticipation of pain and also as a consequence of pain. Thus, as we emphasize later, psychological factors may directly affect nociceptive stimulation and need not be viewed as only reactions to pain.

SOCIAL LEARNING MECHANISMS

Social learning has received some attention in acute pain and in the development and maintenance of chronic pain states. From this perspective, how we experience pain is shaped and influenced by “observational learning”; that is, individuals can acquire responses that were not previously in their behavioral repertoire by watching others perform these activities. Children acquire attitudes about health, health care, and the perceptive style for recognizing and understanding bodily symptoms from their parents and the social environment. They also learn how injuries and diseases should be regarded and addressed. As they grow older, this learning emerges as their tendency to ignore or over-respond to symptoms they experience—the culturally acquired interpretations of symptoms influence how people deal with illness.

There is ample experimental evidence of the role of social learning from controlled laboratory pain studies and some evidence based on observations of patients’ behaviors in field and clinical settings. Physiological responses to pain stimuli may be conditioned during observation of others in pain. For example, patients on a burn unit have sufficient opportunity to observe the responses of other burn patients.²² Each patient’s response is affected by his or her observations of other patients. In one study, children of chronic pain patients chose more pain-related responses to scenarios presented to them than did children with pain-free or diabetic parents. Moreover, teachers rated the pain patients’ children as displaying more illness behaviors (e.g., complaining, days absent, visits to school nurse) than children of pain-free controls.²³ Expectancies as well as actual behavioral responses to noxious stimuli are based, at least partially, on prior social learning history. This may contribute to the marked variability in response to objectively similar degrees of physical pathology noted by health care providers.

A great deal of research has been directed toward explicating the role of cognitive factors in pain. These studies have consistently demonstrated that patients’ attitudes, beliefs, and expectancies about their plight, themselves, their coping resources, and the health care system affect the reports of pain, activity, disability, and response to treatment.^24,25

BELIEFS ABOUT PAIN

Clinicians working with chronic pain patients are aware that patients having similar pain histories and expressions of pain may differ greatly in their beliefs about their pain.²⁶ Behavior and emotion are influenced by how a person interprets events, rather than by objective characteristics of the events. When pain is interpreted as signifying ongoing tissue damage or a progressive disease, such belief often leads to activity avoidance and deactivation in general and is significantly related to greater pain and disability.²⁷ Even for pain-free individuals, belief that the pain is threatening reduces pain tolerance.²⁸ For example, very different responses would be expected of a patient if he attributed his headache to excessive alcohol consumption the night before as opposed to his interpretation that the headache signaled a brain tumor. Thus, although the amount of nociceptive input in the two cases may be equivalent, the emotional and behavioral responses would vary in nature and intensity.

Certain beliefs may lead to maladaptive coping, increased suffering, and greater disability. Patients who believe that there is nothing they can do to control pain may be passive in their coping efforts and fail to make use of available resources to cope with pain. Patients who consider their pain to be an unexplainable mystery feel helpless and clueless as to how to cope with the situation. The sense of helplessness contributes to negative evaluations of patients’ own abilities and coping strategies as effective in controlling and decreasing pain.²⁹ Once beliefs and expectations about a disease are formed, they become stable and are very difficult to modify. Patients tend to avoid experiences that might invalidate their beliefs (disconfirmation), and they tend to guide their behavior in accordance with these beliefs (confirmation), even when the beliefs are no longer valid. A part of the treatment needs to focus on modifying such maladaptive thought processes. For example, therapists may point out that muscular pain following activity may be caused by lack of muscle strength and general deconditioning and not by additional tissue damage. Modification of maladaptive beliefs about their pain seems to predict changes in pain and disability via treatment.³⁰

Chronic low back pain patients generally demonstrate poor behavioral persistence in various exercise tasks, with their performance on these tasks being independent of physical exertion or actual self-reports of pain, but instead related to previous pain reports.³¹ These patients appear to have a negative view of their abilities and expected their pain to increase if they perform physical exercises. Thus, the rationale for their avoidance of exercise was not the presence of pain but their learned expectation of heightened pain and accompanying physical arousal that might exacerbate pain and reinforce their beliefs regarding the pervasiveness of their disability. If patients view disability as an expected consequence of their pain, if they believe that activity is dangerous and that their pain is an acceptable excuse for neglecting responsibilities, they are likely to experience prolonged disability. Patients’ negative perceptions of their capabilities for physical performance form a vicious circle, with the failure to perform activities reinforcing the perception of helplessness and incapacity. Once again, avoidance of activity prevents disconfirmation.

In addition to beliefs about capabilities to function despite pain, beliefs about pain per se appear to be of importance in understanding response to treatment, adherence to self-management activities, and disability.²⁹ When successful rehabilitation occurs, there appears to be an important cognitive shift from beliefs about helplessness and passivity to resourcefulness and ability to function regardless of pain.^24,25

Clearly, it is essential for patients with chronic and recurrent pain to develop adaptive beliefs and to deemphasize the importance of maintaining functionality despite pain. In fact, changes in pain levels do not necessarily parallel changes in other variables of interest, including activity level, medication use, return to work, rated ability to cope with pain, and pursuit of further treatment.³²