Of the earliest theories to explain pain, the psychoanalytic or psychodynamic view postulates that pain originates from psychological mechanisms. This notion has dominated the psychology of pain and has stirred controversy in the field of pain medicine, not only regarding its prevalence, but its very existence [37]. Psychogenic pain is essentially assumed in the absence of organic findings, if the pain is judged to be disproportionate to the physical pathology, or if the symptoms are refractory or unresponsive to standard treatment, then persistent pain is deemed to be primarily due to psychiatric illness.

A number of models of the psychogenic theory have been proposed. The predominant pain-related psychological model was the “pain-prone” personality which described predisposing psychological factors for chronic pain. The pain-prone disorder is characterized by denial of emotional and interpersonal problems, inactivity, depressed mood, guilt, inability to deal with anger and hostility, insomnia, craving for affection and dependency, lack of initiative, and a family history of depression, alcoholism, and chronic pain [38, 39]. This perspective assumes that pain may simply originate from psychological mechanisms, and once the psychic organization necessary for pain is established, the experience of pain no longer requires peripheral stimulation [39]. The model was later modified to suggest that inhibition of affect played a significant role in the etiology of chronic pain [40], and that difficulties in expressing anger and controlling intense emotions are predisposing factors linking chronic pain and negative affect [38, 39].

In the end, the psychoanalytic or psychodynamic theory forms the basis for the distinction of an underlying attempt to identify functional versus organic etiology. Put simply, a dichotomous reasoning is invoked. There is little research to support the etiological role of a pain-prone personality or inhibition of affect in chronic pain states [41]. However, personality attributes such as introversion/extraversion, optimism, perceived locus of control, and personality disorders appear to have a significant effect on patients’ ability to cope with pain [42].

Certain types of stimuli typically elicit specific types of bodily responses. A person blinks when a puff of air is directed at the eye. The pupil of the eye constricts on exposure to bright light. Salivation occurs when food is in the mouth. These and other responses (Table 25.1) are called unconditioned responses (UR). These responses are elicited by antecedent stimuli even though no conditioning or learning has taken place. A UR is a natural reflexive action of the body that occurs when an unconditioned stimulus (US) is presented. URs are common to all people. Respondent conditioning (also called classical conditioning or Pavlovian conditioning) occurs when a previously neutral stimulus is paired with a US (the neutral stimulus and the US are presented together). As a result of this pairing, the neutral stimulus becomes a conditioned stimulus (CS) and elicits a conditioned response (CR) similar to the UR [43].

In acute pain states it may be useful to reduce movement, and consequently avoid pain, to accelerate the healing process. However, in a respondent model of the development of chronic pain, frequent co-occurrence of harmless stimuli, such as activities, body positions, and environments (conditioned stimulus, CS) with acute pain (unconditioned stimulus, US) that may elicit motor, sympathetic, and endocrine responses (conditioned response, CR) may result in a direct relationship between the previously neutral stimuli (activities, body positions and environments) and the physiological responses (motor, sympathetic, and endocrine) [44]. This process of conditioning may lead to a pain-tension cycle that may maintain the chronic pain problem independently from the original tissue damage. Patients may learn to associate increased pain with all kinds of stimuli that were originally associated with nociceptive stimulation [45, 46]. Not only could it be possible for conditioned stimuli to contribute to the maintenance of pain indirectly (through motor, sympathetic, and endocrine systems), but it may also be possible for them to develop maladaptive responses to many stimuli and reduce the frequency of their performance of many activities other than those that initially elicited pain [47, 48].

Operant conditioning (sometimes referred to as instrumental conditioning) is a method of learning that occurs through rewards and punishments for behavior [43]. Through operant conditioning, an association is made between a behavior and a consequence for that behavior. It is distinguished from respondent conditioning (or classical conditioning) in that operant conditioning deals with the modification of “voluntary behavior” or operant behavior. Operant behavior operates on the environment and is maintained by its consequences, while respondent conditioning deals with the conditioning of reflexive behaviors which are elicited by antecedent conditions.

The operant model of chronic pain hypothesizes that the perpetuation of pain behaviors after healing contributes to chronic pain problems and that these behaviors can contribute to suffering and disability [49, 50]. The model focuses on overt pain behaviors (e.g., limping, guarding, rubbing, pain medication use, inactivity) and well behaviors (i.e., adaptive behaviors, such as working and engaging in activities) exhibited by persons with pain (Table 25.2). It is theorized that pain behaviors are natural responses to acute pain that can persist after healing if they are reinforced and if competing well behaviors are not sufficiently reinforced. Over time, this can lead to pain behaviors occurring, at least in part, in response to environmental contingencies and discriminative stimuli (e.g., spouses, other family members, or healthcare providers who might reinforce pain behaviors) instead of only in response to nociception. For the most part, such behaviors involve limiting one’s activity and functioning.

Although operant factors undoubtedly play a role in chronic pain, a fundamental problem with the operant approach is its emphasis on the communicative role of pain behaviors rather than on pain itself. According to this approach, observed behaviors are used as the basis to infer something about the internal state of the person. The observer may infer that certain behaviors are communications of pain, distress, and suffering. However, there is no way to determine from the behavior alone whether it results from pain, conditioning, structural abnormality, adherence to provider recommendation, pacing of activities, or whether it is a coping response. Unless observers ask patients why they are engaged in a certain behavior, they cannot know the motivation for the behavior.

Social learning theory is a perspective that states that people learn within a social context. It is facilitated through concepts such as observational learning, or modeling, and is an essential mechanism of learning new patterns of behaviors [51]. Individuals acquire perceptions and interpretations of symptoms and physiological processes from modeling and observations in their social environment. They also learn appropriate responses to injury and disease and consequently may be more or less likely to under or overrespond to the normal physical sensations they experience. A large number of studies have shown that physiological responses to pain stimuli may be vicariously conditioned during observations of others in pain [52] and that modeling can influence the expression and localization of pain and pain-coping behaviors, and pain perceptions in others activate both automatic and controlled processes [53].

Investigations of social learning have indicated that observational learning influences both observable expression of acute pain as well as the subjective experience [54]. In an experimental study, children observing their mothers’ reactions during painful exposure of the hand to cold water subsequently displayed lower pain thresholds when their mothers had voluntarily exaggerated their pain [55]. Furthermore, children displayed reduced facial displays of pain when the mother had voluntarily suppressed her reaction. Instructive studies that examined observational learning of pain-related fear [56, 57], provided substantial evidence of the powerful impact that observing others in pain had on neurophysiological activity in observers. However, the broader mechanisms whereby observational learning plays a crucial role in establishing pain-related responses remain relatively uninvestigated; no systematic research is available examining cognitive and affective mechanisms (e.g., changes in beliefs about pain and attitudes toward pain) underlying the effects on behavior, including the moderators of these effects. Despite the great deal of data available on the modification of experimentally induced pain behaviors by means of modeling in normal (healthy) people, there are few experimental results concerning chronic pain patients.

A growing body of literature has focused on the interaction between depression and pain symptoms. This interaction has been labeled by some authors as the depression–pain syndrome [58] or depression–pain dyad, implying that the conditions often coexist, respond to similar treatments, exacerbate one another, and share biological pathways and neurotransmitters [59, 60]. Patients with depression often present with a complex set of overlapping symptoms, including emotional and physical complaints. Physical complaints typically include medically unexplained pain [61].

Although it is generally understood that depression and painful symptoms are common comorbidities, the extent to which depression and chronic pain are associated remains a contentious issue that empirical studies have failed to resolve it completely. Evaluation of the relevant literature provides increased support for an association between chronic pain and depression and suggests that coexisting syndromes may be a final common presentation [62]. However, in most cases, depression appears to be more of reaction to the condition [63].

Comorbidity between anxiety disorder and pain seems to be prevalent [64]. Studies conducted among selected groups of respondents have found the presence of pain to be associated with anxiety symptoms [65]. More specifically, there is ample evidence indicating that fear and avoidance are crucial factors not only in acute pain but in chronic pain [46]. Researchers have also found a close association between fear of pain and dysfunctional coping [66, 67] with muscle hyperactivity in response to stress being closely associated with the fear of pain [68]. Evidence from large epidemiologic studies suggests that the association of anxiety disorders with chronic pain is comparable to other mood disorders. The link between anxiety disorders and chronic pain, when they co-occur, is often complex and may not always lend itself to a simple cause-and-effect relationship, as both conditions may have a shared distal, rather than a proximal origin.

Anger has long been recognized as an integral part of pain experience [69, 70]. It has been discussed as an aversive emotional state ranging from mild irritation to fury [71], and comprising specific cognitive attributions and action tendencies [72, 73]. Anecdotal and empirical data suggest that anger is commonplace among chronic pain sufferers [74] and that inhibiting anger expression may amplify acute and chronic pain at a later time [75]. Studies have consistently indicated that greater trait of anger is associated with elevated acute and chronic pain responsiveness [76–78]. In other studies, increased sensitivity to acute pain was found, in roughly equal degrees, among participants who claim to become easily angered, those who claim that they bottle up their anger, and those who claim that they vent their anger more explosively [40, 79, 80].

Beliefs have been defined as personally or culturally shared cognitive configurations [81] that may be generalized or specific to certain contexts, mold the individual’s perception of the environment, and shape the meaning of their experiences [82]. It has been suggested that beliefs about persistent pain have two dimensions. These dimensions are organic pain beliefs (the physiological experience of pain) and psychological pain beliefs (the internal influences and feelings of the experience of pain) [83]. Both dimensions can potentially influence viewpoints about pain control either positively (having personal control over the pain experience) or negatively (feeling helpless to manage the potential threat to their well-being).

Research shows that negative pain beliefs have a detrimental impact on patients’ overall health, self-efficacy, and function [84]. A number of studies reported that negative pain beliefs can contribute to the transition from acute pain to persistent pain [81, 85]. Beliefs of physical capabilities and not the experience of self-reported pain, appears to affect physical functioning and contributes to disability [84–86]. Conviction of personal control was shown to ameliorate the experience of experimentally induced nociception in a study that used experimental pain stimuli [87]. Specific pain beliefs that contribute to poor compliance, motivation, and misunderstanding about pain have been identified. These include catastrophizing, limited perception of control over the pain experience, and emotional distress [85] with evidence that addressing negative pain beliefs in the management of persistent pain can affect treatment outcomes [88–90].

Based on the theory of social learning, self-efficacy describes the confidence the person has in his or her own ability to achieve a desired outcome [91]. Higher levels of self-efficacy have been found to be associated with lower levels of pain and disability in patients with chronic pain [92–94]. In a study by Dolce et al. [95], self-efficacy was found to be related to exercise performance in chronic pain patients. In their study, they found that beliefs regarding ability to exercise predicted improvements in work status and exercise level 6–12 months after a physical reactivation program. In another study, researchers demonstrated that pain-related self-efficacy ratings are likely to change following cognitive-behavioral management and that these changes were associated with better outcomes such as reduced disability [96, 97]. In a study that asked patients to rate their self-efficacy and expectancy on performance of movement tasks, performance levels were highly related to their self-efficacy expectations, which in turn appeared to be determined by their expectancy of pain levels [98]. A number of other studies have reported that success in response to rehabilitation was predicted by perceived self-efficacy [99, 100].

The term catastrophizing was formally introduced by Albert Ellis [101] and subsequently adapted by Aaron Beck [102] to describe a maladaptive cognitive style employed by patients with anxiety and depressive disorders. At the core of their definitions of catastrophizing was the concept of an irrationally negative forecast of future events. Similarly, pain-related catastrophizing is broadly conceived as a set of exaggerated and negative cognitive and emotional schema brought to bear during actual or anticipated painful stimulation [103, 104].

The catastrophizing literature to date provides rather demonstrative evidence for the influence of catastrophizing in shaping emotional, functional, and physiological responses to pain, and was found to be the strongest pain predictor, followed by pain-related fear and bodily vigilance [105]. Catastrophizing has been shown to be associated with persistent pain and to be a predictor of poor outcomes in pain management interventions [89, 106]. The literature also points to consistent and generally robust associations between pain catastrophizing and an array of clinical pain-related outcomes, including measures of clinical pain severity, pain-related activity interference, disability, depression (and other negative mood indices), and alterations in social support networks [107, 108]. Moreover, catastrophizing has been linked to increased behavioral expressions of pain, as well as a variety of illness behaviors (e.g., more frequent visits to healthcare professionals). It is important to note that the magnitude of these relationships is variable, with catastrophizing accounting for minimal variance in pain severity in some studies, and up to 31 % of the variance in pain severity in others [107].

Acceptance is emerging as a potentially valuable concept in contemporary theories of how patients react and adapt to chronic pain. It denotes a state of mind where a person is aware of the pain but does not try to actively change or avoid it [109, 110]. In a study examining patients awaiting interdisciplinary treatment, researchers found that acceptance of chronic pain was more successful in predicting pain, depression, disability, pain-related anxiety, and patient physical and vocational functioning than were measures of coping [111]. A host of studies demonstrated that acceptance is associated with better physical, social, and emotional functioning, in work-related functioning, and in analgesic and healthcare use [112–115]. Other studies have shown convincingly that acceptance of chronic pain is associated with reports of less pain, psychological distress, and physical and psychological disability, as well as more daily up time [112, 116].

Three professional biofeedback organizations, the Association for Applied Psychophysiology and Biofeedback, Biofeedback Certification International Alliance, and the International Society for Neurofeedback and Research, arrived at a consensus definition of biofeedback in 2008 [120].

Biofeedback is a process that enables an individual to learn how to change physiological activity for the purposes of improving health and performance. Precise instruments measure physiological activity such as brainwaves, heart function, breathing, muscle activity, and skin temperature. These instruments rapidly and accurately ‘feedback’ information to the user. The presentation of this information—often in conjunction with changes in thinking, emotions, and behavior—supports desired physiological changes. Over time, these changes can endure without continued use of an instrument.

Simply put, biofeedback is a means for gaining control of our physiological functioning (e.g., skin temperature, muscle tone, skin conductance, heart rate) primarily using instruments that provide information (e.g., visual) on the activity of those same systems with a goal of being able to manipulate them at will. Although not always the case, biofeedback may typically include training in relaxation procedures.

The biofeedback literature on chronic abdominal pain is limited and primarily based on IBS studies. Some studies have been promising, but the most current review indicated that there was insufficient evidence to support the use of biofeedback for some GI conditions [121]. The review concluded that the evidence is insufficient to support the efficacy of biofeedback for constipation, encopresis, fecal incontinence, and abdominal pain. However, a study using thermal biofeedback and diet (increased fiber) was shown to be effective and efficient as a treatment modality for recurrent abdominal pain [122]. Forehead Electromyographic (EMG) biofeedback and thermal biofeedback have shown some benefits to counteract the effects of stress in patients with IBS [123]. EMG biofeedback demonstrated benefits on reduction of constipation [124–126], but a multicomponent behavioral intervention for IBS that included thermal biofeedback was not more effective than an attention-control intervention [127]. Relaxation training, involving progressive muscle relaxation, thermal biofeedback, cognitive therapy, and education, implemented through biofeedback training in patients with IBS was found to be more effective than the control group (waiting list) in reductions in GI symptoms (e.g., abdominal pain, constipation, and diarrhea) [128–130]. However, wait-list control groups do not adequately control for expectancy (placebo), and such experimental designs may overestimate treatment effects. Biofeedback therapy using breathing exercises on autonomic imbalance in patients with functional dyspepsia improved tolerance to water intake and improved quality-of-life scores, but clinical outcome and control treatment were both poorly defined [131]. Ability to significantly influence gastric contraction was demonstrated after 4 h of heart beat biofeedback training [132]. Although it is possible to teach individuals to alter their gastric motility, the clinical utility of research protocols aimed at influencing gastric motility has yet to be established.

According to the American Society of Clinical Hypnosis, “Hypnosis is a state of inner absorption, concentration and focused attention.” [133]. While there is general agreement that certain effects of hypnosis exist, there are differences of opinion among research and clinical communities about how analgesic hypnosis works. Some researchers generally describe hypnotic analgesic interventions as including the induction of relaxed states of focused attention and inner absorption, with a relative suspension of peripheral awareness, combined with suggestions for analgesia [134].

Hypnotherapy has been shown to be a strongly supported psychological intervention for IBS with at least three separate randomized controlled trials supporting its efficacy in reducing symptomatology and improving quality of life [135]. In a systematic review, hypnotherapeutic interventions showed long-lasting symptom relief with influences on colorectal sensitivity, colorectal motility, and mental strain (anxiety, depression, maladaptive cognitions) [136]. In another review, the authors concluded that hypnosis consistently produced significant results and improved the cardinal symptoms of IBS in the majority of patients, as well as positively affecting non-colonic symptoms [137]. Hypnotherapy also normalized visceral pain thresholds in IBS patients; threshold-associated changes were highly correlated with improvement in clinical symptoms [138]. In addition, hypnotherapy demonstrated reduced sensory and motor components of gastrocolonic responses in patients with IBS [139]. Hypnotherapy studies with IBS patients have yielded promising results, however, the underlying mechanisms of action are not well understood. Hypnotherapy appears to maintain its long-term benefits quite well, with 81 % maintaining improvements in IBS symptoms for up to 5 years [140].

Cognitive behavior therapy (CBT) is a type of psychotherapeutic treatment that helps patients understand thoughts and feelings that influence behaviors. The underlying concept behind CBT is that one’s thoughts and feelings play a fundamental role in behavior. Cognitive behavior therapy teaches patients a blend of behavioral skills (e.g., relaxation and pain-coping skills training) and cognitive therapy (e.g., restructuring negative cognitions such as catastrophizing) with the goal of reducing pain, pain-related disability and distress, as well as increasing self-efficacy [141].