The psychobiology of chronic pain

Adv. Behov. Res. Thu. Vol. 12, pp. 47-84, 1990. Printed in Great Britain. All rights reserved.

THE PSYCHOBIOLOGY

0

OF CHRONIC

Herta Flor,* Niels Birbaumer,*

0146-6402/90 $0.00+.50 1990 Pergamon Press plc.

PAIN

and Dennis C. Turk?

*Abteihmg Klinische und Physiologische Psychologie, Universitlt Tiibingen, F.R.G. tPain Evaluation and Treatment Institute, University of Pittsburgh School of Medicine, U.S.A. Abstract - Biomedical and psychological perspectives on chronic pain have each advanced our understanding of the development and maintenance of chronic pain syndromes and have led to more effective assessment and treatment approaches. Little attention, however, has been given to the development of a comprehensive model that integrates both biomedical and psychological variables in the etiology, maintenance, and exacerbation of chronic pain. The purpose of this article is to propose a dynamic psychobiological model of chronic pain that emphasizes the interaction among psychological and biomedical variables. The experience of pain is viewed as a complex response that incorporates subjective-psychological, motor-behavioral, and physiological-organic components. Moreover, we postulate that there are varying degrees of synchrony among responses’measured on these levels determining the development and etiology of chronic pain syndromes. Specifically, we propose that the development and maintenance of chronic pain is a function of several interacting components: (a) a predisposition to respond with a specific bodily system, (b) external or internal aversive stimulation, (c) maladaptive information processing of and coping with pain-related social and/or physiological stimuli, and (d) operant, respondent, and observational learning processes.

INTRODUCTION Despite the significant advances in modern medicine, pain, specifically pain that has persisted beyond the expected period of healing or that is the result of a progressive disease (i.e., chronic pain) or that recurs intermittently (e.g., migraine headache), has remained a puzzle and has proven recalcritant to traditional medical treatment methods (Hilgard, 1969; Melzack & Wall, 1983). A major contributor to the current state is the fact that until recently the conventional view of pain considered reports of pain exclusively as a by-product and symptom of physical

The completion of this article was supported by grants # Fl 156/l and Fl 156/2 from the Deutsche Forschungsgemeinschaft to the first, grant # 0701503 from the Bundesministerium fiir Forschung und Technologie to the second, and grants # ROl DE 07514 from the National Institute of Dental Research and ARNS 38698 from the National Institute of Arthritis, Musculoskeletal and Skin Disease to the third author. The authors are solely responsible for the contents of the publication. Address all correspondence to: Herta Flor, Abteilung Klinische und Physiologische Psychologie der Universitlt Tiibingen, GartenstraSe 29, D-7400 Tubingen, Federal Republic of Germany.

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pathology directly related to tissue damage, and primarily a sensory experience. Pain in its own right has only been viewed as a problem worthy of consideration during the past quarter century. The failure of conventional medical treatments to consistently and permanently alleviate reports of pain has resulted in the development of a plethora of alternative treatment approaches. These treatment approaches have evolved largely on an empirical basis, often without a theoretical rationale. Recent multidimensional (e.g., Melzack & Wall, 1965) and behavioral models (cf., Fordyce, 1976) have advanced our understanding of the range of psychological and physiological factors that contribute to the experience and report of chronic pain. Often, medical and behavioral views of chronic pain have been contrasted without consideration of the many interactions among biological and psychological processes. Few attempts have been made to consider how the physiological and psychological data might supplement each other to produce a more comprehensive model (Price, 1987). In practice, although physiological and psychological research on chronic pain has mushroomed in recent years the different areas of research have been conducted in relative isolation. There is little collaboration between the biomedical and behavioral sciences in the area of basic research or the integration of psychological and physiological knowledge. This problem of inadequate, single factor models is not unique to pain: it is quite prevalent in explaining chronic illnesses in general (e.g., McHugh & Vallis, 1987). A prime example of this is the polarization in psychiatry and psychopathology between psychogenic and neurophysiological or biochemical models. There is now increasing evidence that there may be a set of interrelated etiological and maintaining factors in psychopathology. This has been most evident in psychophysiological disorders (Cohen, 1979). The purpose of this paper is to propose a psychobiological view of chronic pain that brings together the various models that have been developed to describe the role of psychological factors with the physiological processes involved in chronic pain states. We will attempt to integrate the existing physiological and psychological knowledge. Most of what we propose is speculative and thus must be viewed as tentative. However, detailed specification of this model will permit empirical investigation and refinement based on research. It is our view that presenting the model as explicitly as possible will instigate direct empirical examination of the role of learning processes and their interaction with physiological processes in chronic pain. We hope that this discussion will serve as an impetus for more collaborative research that will facilitate understanding of the many interrelated factors in the development, maintenance, exacerbation, and subsequently the treatment of chronic pain. Before we discuss the main components of a psychobiological view of chronic pain, we will briefly review current conceptualizations of pain.

Psychobiology of Pain

BRIEF

OVERVIEW

OF CURRENT

49

CONCEPTUALIZATIONS

Pain is essential for survival because of its alarm function. In acute pain states nociception acts as a signal that requires immediate attention and action in order to prevent further damage and to facilitate the healing process. In chronic pain this adaptive function plays a significantly smaller role and can often no longer be discerned. Chronic pain may not be connected to or may be disproportionate to the extent of tissue damage, in many cases no longer functions as a sign of an underlying disease process, and may thus become a problem in its own right (Osterweis, Mechanic, & Kleinman, 1987).

Unidimensional

Sensory Model

At least since the time of the ancient Greeks, pain has been viewed as a specific sensory experience in the same way vision or olfaction are viewed as sensations, The traditional unidimensional model of pain adhered to a specificity concept postulating that pain is a specific sensation and that pain intensity is directly proportional to the amount of peripheral nociceptive input related to tissue damage (Melzack & Wall, 1983). It was assumed that some form of tissue damage would excite receptors that were specific, responding exclusively to nociceptive stimuli initiating pain-specific nerve impulses that were transmitted along specific pain pathways to a specific pain center localized in the brain where the experience of pain would then motivate actions to avoid further harm. There has been accumulating evidence that mitigates against the validity of this model. Furthermore, medical treatments have shown that this unidimensional concept is inadequate. Specifically, neurosurgical attempts at the alleviation of chronic pain by the blockage of sensory input from nociceptors or its transmission along the spinal cord by surgical interference with nociceptive transmission have often proven not to eliminate pain, to eliminate pain only for short periods of time, or elicited new types of pain and exacerbated the problem (cf., Loeser, 1980). A large body of laboratory data reveals that even in acute laboratory pain, pain and nociceptive input do not have an isomorphic relationship. Rather, a host of factors modulate the perception of pain, among them most prominently cognitive variables such as attention and the perception of control as well as affective variables such as anxiety (cf., Turk, Meichenbaum, & Genest, 1983; Weisenberg, 1977; Craig, 1989). More recent conceptualizations view pain as a perceptual process resulting from the nociceptive input and its modulation on a number of different levels in the central nervous system (Melzack, 1986) and not as directly proportional to nociceptive input.

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The Gate Control Model

Multidimensional views of chronic pain differentiate nociception, that is processing of stimuli that are defined as related to the stimulation of nociceptors and capable of being experienced as pain, from pain that is a psychological phenomenon comprised of the integration and modulation of a number of afferent and efferent processes (Melzack, 1986). The complex interplay of the action of receptors, afferent and efferent neurons, spinal, as well as supraspinal processes contribute to the experience of pain, which need not be equated with peripheral stimulation. Based on this view, Melzack and Wall (Melzack & Wall, 1965; Wall, 1978) proposed the gate control theory of pain. They postulated the modulation of the nociceptive input by afferent as well as efferent mechanisms, converging on the dorsal horn substantia gelatinosa, which was suggested to act as a gate, involving presynaptic and postsynaptic inhibitory mechanisms. Furthermore, Melzack and Casey (1968) and Melzack and Wall (1965) differentiated three systems related to the processing of nociceptive stimulation a motivational-affective, sensory-discriminative, and cognitive-evaluative dimension - that were all thought to contribute to the experience of pain. Recently, Wall (1988) has emphasized that in addition to the mechanism of gate control, slower acting mechanisms of sensitivity and connectivity control may modulate nociceptive input. The multidimensional conceptualization of pain, as described in the conceptual model of the gate control theory, emphasizes the modulation of pain by peripheral as well as central nervous system processes and thus provides a physiological basis for the role of psychological processes in chronic pain states. Although physiological details of this model have been proven to be problematic (cf., Nathan, 1976; Price, 1987; R.F. Schmidt, 1972), it has had a substantial impact on the development of psychological methods for pain control (Turk et al., 1983). The gate control model was developed as a static cross-sectional view; consequently it has not considered the role of reinforcement and learning factors that are salient if one takes a dynamic longitudinal view of pain. The gate control model is also silent concerning the modes of interaction among behavioral and biological variables. Physical versus “Psychological”

(“Psychogenic”)

Pain

Throughout the history of pain research there have been attempts to distinguish a sensory or physiological from a reactive or emotional or psychological component of pain (cf., Barber & Hahn, 1965; Rachlin, 1985) or to differentiate somatogenic and psychogenic pain. The concept of psychogenic pain and its psychoanalytic interpretation

Psychobiology of Pain

as conversion hysteria (cf., Freud, “organic” and “psychological” pain. of pain never received much empirical Similarly, the revised edition of the

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1952) is based on this dualism of However, psychodynamic concepts support (cf., Turk & Salovey, 1984). Diagnostic

and Statistical Manual

of

(DSM III-R, American Psychiatric Association, 1987) differentiates somatogenic from somatoform (formerly “psychogenic”) pain. The definition of somatoform pain in DSM III-R depends on (a) either the lack of organic findings to explain the present pain, or (b) a discrepancy of organic findings and pain complaints and the identification of psychological causation. This is a problematic definition because it defines the presence of a psychological problem on the basis of the absence of somatic findings and retrospective identification of psychological factors that putatively have an etiological role in the reports of pain. Moreover, there is no exact definition of the nature of organic findings that would be expected nor is the fact considered that many pain-eliciting processes may not present themselves as organically demonstrable physical findings. The somatogenic-psychogenic categories are necessarily dichotomous, thus oversimplifying the contribution of the many factors involved in the experience of pain. This view also overlooks that the factors related to the causation may differ from those related to the maintenance of a pain problem. the American

Psychiatric Association

Operant Perspective of Pain

A new era in psychological approaches to pain began with Fordyce’s work on behavioral factors in chronic pain. The operant model as formulated by Fordyce (1976) distinguishes between the private pain experience and observable and quantifiable “pain behaviors.” Only the latter are assumed to be amenable to behavioral assessment and treatment. The model proposes that acute pain behaviors such as limping to protect a wounded limb from producing additional nociceptive input may come under the control of external contingencies of reinforcement and thus develop into a chronic pain problem. Pain behaviors (e.g., complaining, inactivity) may be positively reinforced directly, for example, by attention from a spouse or medical personnel. Pain behaviors may also be maintained by the escape from noxious stimulation by the use of drugs or rest, or the avoidance of undesirable activities such as work or unwanted sexual activity. In addition, “well behaviors” (e.g., working) may not be sufficiently reinforcing and the more rewarding pain behaviors may, therefore, be maintained. Thus, the pain behavior originally elicited by organic factors may come to occur, totally or in part, in response to reinforcing environmental events. Because of the consequences of specific behavioral responses, it is proposed that

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pain behaviors may persist long after the initial cause of the pain is resolved or greatly reduced. Fordyce’s operant conditioning model was proposed in direct response to the apparent lack of efficacy of the traditional medical approaches in ameliorating chronic pain and has generated what appears to be an effective treatment approach for pain behaviors (cf., Linton, 1986; Malone & Strube, 1988; Turner & Romano, 1984; Keefe & Williams, 1989). The operant approach has, however, been criticized for its exclusive focus on motor pain behaviors and its failure to consider the emotional and cognitive aspects of chronic pain (cf., A.J.M. Schmidt, 1985; A.J.M. Schmidt, Gierlings, & Peters, 1989). Moreover, it has not been investigated to what extent the operant approach is applicable to pain problems with a predominantly physical cause (e.g., cancer-related pain). Respondent Conditioning Respondent conditioning, specifically the existence of a pain-tension cycle, has received some attention in chronic pain research (Gentry & Bernal, 1977). Although assumptions about increased muscle tension levels in chronic pain have been the basis for the biofeedback treatment of headaches or back pain, theoretical assumptions about their role in the maintenance of pain have surfaced only recently. For example, Lethem, Slade, Troup, and Bentley (1983) and Linton, Melin, and Gotestam (1985) have ‘suggested that once an acute pain problem exists, fear of motor activities that the patient expects to result in pain may develop and motivate avoidance of activity. Philips (1987) has specifically emphasized how pain behaviors may be maintained by avoidance learning. In acute pain states avoidance behaviors may be protective and adaptive, however, over time these responses may inhibit the return to a non-pain state. For example, reduction in physical and social activity may subsequently result in muscle atrophy, increased impairment, greater disability as well as depressed mood. A.J.M. Schmidt (cf., Amtz & A.J.M. Schmidt, 1989) has specifi-’ tally suggested that the processing of internal stimuli may be disturbed in chronic pain patients. Linton et al. (1985) have provided a more detailed account of the processes .involved in classical conditioning of chronic pain but there is still a lack of empirical research concerning these mechanisms. Social Learning

Another learning mechanism that has received some attention in the development and maintenance of chronic pain states is the acquisition of pain behaviors by means of social learning or modeling processes. That is, individuals can acquire responses that were previously not in their behav-

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ioral repertoire by the observation of others performing these activities. Bandura (1969) has described and documented the important role of observational learning in many areas of human functioning. The observation of others in pain is an event that captivates attention. This attention may have survival value, may help to avoid experiencing more pain and help to learn what to do about acute pain. There is ample experimental evidence of the role of social learning from acute pain experiments (Craig, 1986,1988) but most of the evidence on chronic pain is correlational, often retrospective. Cognitive-Behavioral

Perspective

Recently, the role of cognitive factors has been emphasized in the maintenance of chronic pain (Turk et al., 1983). From the cognitive-behavioral perspective, people with chronic pain are viewed as having negative expectations about their own ability to control certain motor skills without pain (A.J.M. Schmidt, 1985). Moreover, chronic pain patients tend to believe that they have limited ability to exert any control over their pain. Such negative, maladaptive appraisals about the situation and personal efficacy may reinforce the experience of demoralization, inactivity, and overreaction to nociceptive stimulation (Biedermann, McGhie, Monga, & Shanks, 1987; Brown & Nicassio, 1987; Demjen & Bakal, 1986). These cognitive appraisals and expectations are postulated as having an effect on behavior leading to reduced effort and activity that may contribute to increased psychological distress (helplessness) and subsequently physical limitations (Philips, 1987). Although the cognitive-behavioral view has emphasized the important role of cognitive processes for coping with chronic pain, it has not sufficiently integrated the theoretical concepts and empirical research on information processing and memory in current cognitive psychology (Rumelhart & McClelland, 1986). Conclusions

Overall, much progress has been made in delineating the factors that may contribute to chronic pain. However, with the exception of the gate control model, these conceptions have adhered to a dualistic view and have dichotomized pain into sensory and emotional or somatogenic and psychogenic (Rachlin, 1985). All the models that were described above have received some empirical evidence supporting them but there has so far been a lack of integration as well as specificity of mechanisms. That is, several biomedical and psychological factors have been held responsible for the development of chronic pain syndromes but they have usually been conceptualized as competing models. Moreover, these approaches have usually focused on one aspect of the latent construct of pain, such as

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physiological processes, pain behaviors, or pain-related cognitions without specifying their interactions and their developmental aspects. THE PSYCHOBIOLOGICAL

PERSPECTIVE

A multifactorial dynamic view of chronic pain is proposed that incorporates the mutual interrelationship of physiological and psychological factors and the change of these interrelationships over time. Several authors (e.g., Bakal, 1982; Bischoff & Traue, 1983; Feuerstein, Papciak, & Hoon, 1987) have described a biobehavioral conceptualization of chronic pain states. None of these models, however, has been specific with respect to the role of learning and the biobehavioral interactions in chronic pain. We view pain as a response with physiological, behavioral and subjective components, that may or may not have an underlying organicpathological basis in the sense of a structural change, but that will always have physiological antecedents and consequences. That is, behavior is also physiological and physiological processes have behavioral expressions. Birbaumer (1984, 1986; Birbaumer & Flor, in press) has emphasized this trimodal conceptualization of pain that includes verbalsubjective, behavioral-motor, and physiological components. The physiological level incorporates ascending and descending neuronal processes, supraspinal and cortical mechanisms, as well as neurochemical processes. The verbal-subjective modality includes thoughts, feelings, and images. The behavioral-motor level includes pain behaviors ranging from medication intake to grimacing and use of the health care system (Turk & Flor, 1987). Interactions are continuous - learning occurs in physiological mechanisms, and physiological mechanisms are modified by behavioral changes. Thus, pain behaviors may be motivated by both physiologial and behavioral antecedents and consequences and both need to be considered in the analysis of pain. This view is consistent with the IASP (International Association for the Study of Pain, 1986) definition that views pain as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (p. 217) but, in addition, emphasizes behavioral parameters as integral to the experience of pain on the subjective and bodily level. Basic Components

in the Development

of Chronic Pain

The focus of this section is on the development of chronic pain states. Whereas everyone experiences acute pain, only a small percentage of patients develop chronic pain syndromes. It is suggested that preconditions for chronic pain include several components: (1) Predisposing Factors: The existence of a physiological predisposi-

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tion or diathesis involving a specific body system. This predisposition consists of a reduced threshold for nociceptive activation that may be related to genetic variables, previous trauma, or social learning experiences and results in a physiological response stereotypy of the specific body system. (2) Precipitating Stimuli: The existence of persistent aversive external and/or internal stimuli (pain-related or other stressors) with negative meaning that activate the sympathetic nervous system and/or muscular processes (e.g., various aversive emotional stimuli such as familial conflicts or pressures related to employment) as unconditioned and conditioned stimuli and motivate avoidance responses. Aversive stimuli may be characterized by “excessive” intensity, duration, or frequency of an external or internal stimulus. (3) Precipitating Responses: “Inadequate” or “maladaptive” behavioral, cognitive or physiological repertoire of the individual to reduce the impact of these aversive environmental or internal stimuli. An important role is played by the cognitive processing of external or internal stimuli related to the experience of stress and pain: for example, increased perception, preoccupation and overinterpretation of physical symptoms or inadequate perception of internal stimuli such as muscle tension levels. Moreover, the nature of the coping response - active avoidance, passive tolerance, or depressive withdrawal may determine the type of problem that develops as well as the course of the illness. Subsequent maladaptive physiological responding such as increased and persistent sympathetic arousal and increased and persistent muscular reactivity may induce or exacerbate pain episodes. (4) Maintaining Processes: Learning processes in the form of classical conditioning of fear of activity (including social, motor, and cognitive activities) and operant learning of pain behaviors - but also operant conditioning of pain-related covert and physiological responses as described above - make a contribution to chronicity. We have summarized the main factors that we believe to contribute to the development and maintenance of chronic pain and will describe these factors and their potential interactions in more detail in the following section. It is important to note that these four components were separated to simplify discussion; they do, however, interact and are not mutually exclusive or intended to connote a linear sequence. We will delineate possible mechanisms involved in the development of chronic pain - both pain following injury and gradually evolving pain states. The psychobiological model described deals primarily with typical musculoskeletal pain syndromes such as headaches, back pain, temporomandibular pain and pain in the rheumatic diseases, by far the most common chronic pain syndromes (Burrows, Elton, & Stanley, 1987; Fields, 1987). .MmT 12:2-n

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The Role of Predisposing

Variables

Genetic factors

Genetic factors have been implicated in a number of chronic pain syndromes, although the empirical evidence for their role is scarce. In pain states not related to acute trauma, genetic predisposition may play a role in the location of the pain as has been suggested in some types of migraine headaches (cf., Bille, 1981). There is some evidence from animal research that rat strains may display natural variations in autotomy following nerve injury (Inbal, Devor, Tuchendler, & Lieblich, 1980) that may be a genetically determined fact, and that strains with differential sensitivity to pain may be bred (Devor, Inbal, & Govrin-Lippman, 1982). Veterinarians have noted that some animal strains (certain dogs) and species (horses) are predisposed to develop chronic back pain. There have also been reports of congenital insensitivity to pain (Sternbach, 1963) although congenital hypersensitivity has not been observed (Comings & Amronin, 1974). Droste and Roskamm (1983) suggested that possibly genetically determined individual differences in endorphinergic mechanisms may play a role in differential sensitivity to pain in patients suffering from myocardial ischemia. They compared patients with symptomatic and asymptomatic myocardial ischemia and found significantly higher electrical and chemical pain thresholds as well as more cold pressor pain tolerance in the asymptomatic patients.

Learning

as a predisposing factor

Children acquire attitudes about health and health care, the perception and interpretation of physical symptoms and physiological processes from their parents and social environment as well as appropriate responses to injury and disease and may thus be more or less likely to ignore or overemphasize symptoms they experience (cf., Mechanic, 1983; Pennebaker, 1982). This culturally acquired perception and interpretation of symptoms determines how people deal with illness (Nerenz & Leventhal, 1983). For example, Rickard (1988) found that children of chronic pain patients chose more pain related responses to scenarios presented to them and were more external in their health locus of control scales than children with healthy or diabetic parents. Moreover, teachers rated the pain patients’ children as displaying more illness behaviors (e.g., complaining, crying, whining, avoidance, dependency, days absent, visits to school nurse) and as more behaviorally deviant. Similarly, Christensen and Mortensen (1975) reported that children are more likely to acquire the type of pain syndromes their parents have in adulthood, not those their

Psychobiology of Pain

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parents had in childhood. These data are suggestive and provide some support to the potential of ohervutional Zeurning as an etiological factor. As noted previously, Craig (1986) has reported a large body of evidence for the importance of observational learning in pain tolerance, pain ratings, as well as non-verbal expressions of pain. For example, Vaughan and Lanzetta (1980, 1981) demonstrated that physiological responses to pain stimuli may be vicariously conditioned during observations of others in pain. Block (1981) showed that spouses of pain patients respond with physiological activation to viewing their patient spouses in pain. This physiological activation may instigate symptoms in the spouses. There is evidence that the observation of pain in other family members may predispose individuals to similar pain problems (Apley & Hale, 1973; Christensen & Mortensen, 1975; Turkat, Kuczmierczyk, & Adams, 1984) thus implicating a learning process in the development of a diathesis. There have been suggestions that a predisposition towards hyperreactivity to nociceptive input may be related to a luck of exposure to pain stimuli eurfy in life. This is especially evident in ethnomedical observations of certain populations. Early desensitization to traumatic injury through rituals such as the severing of the ear lobes or nose at a young age seem to leave the young less susceptible to later trauma. For example, Schiefenhovel’s (1980) observations of pain tolerance and pain behaviors among the Eipo tribe or Sargent’s (1984) studies of the Bariba in Benin and Nigeria in New Guinea suggest that early and negative experience with painful stimulation reduces the expression and possibly the experience of pain and suffering in adults as compared to Western cultures. Conversely, there is some, however controversial, evidence that some breeds of dogs and monkeys that were not exposed to painful stimulation were insensitive to pain stimuli and unable to learn avoidance responses to nociceptive stimuli (Lichstein & Sackett, 1971; Melzack & Scott, 1957). The occurrence of uncomrolf&e pain-related traumatic events may also increase the likelihood of physiological overreactivity in a certain body part. For example, Harvey and Greer (1982) noted that unpredictable shock to a limb leads to an anticipatory stiffening of the limb to reduce the impact of the aversive stimulus. Similar responses could occur in children exposed to physical abuse. A higher prevalence of physical abuse in childhood is often reported in certain types of chronic pain (Violon, 1985). The results of a study by Morpurgo, Gavazzi, Pollin, Amsallem, and Lombard (1983) provide experimental evidence for this assumption. These authors showed that the brains of kittens exposed to pain stimuli showed much larger receptive fields of the affected body part in the thalamus and cortex. This might provide a physiological basis for vulnerability of certain body parts based on early trauma. Further predisposing trauma might be related to occupational factors.

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These results seemingly contradict the assumption that early exposure to painful stimulation may be necessary for adequate pain responses to develop. It is, however, possible that these conflicting results are related to the controllability and intensity of the noxious stimulation. Moderate levels of noxious stimulation in a controllable situation combined with social disapproval for the expression of pain behaviors and approval for coping as reported for the children of the Eipo tribe (Schiefenhovel, 1980) may result in different physiological and psychological consequences as compared to the uncontrollable noxious stimulation to which battered children are exposed.

Occupational

factors

An additional mechanism occurring in later life that could be predisposing to the development of chronic pain includes occupationaZ factors. For example, constant overuse of a specific body part may make the musculature and joints more susceptible to nociceptive responding (Schtildt, Ekholm, Harms-Ringdahl, Arborelius, & Nemeth, 1987). Musicians are known to develop instrument-specific pain syndromes (Newmark & Hochberg, 1987) and “repetitive strain injury” has been described as a new epidemic in Australia (Kiesler & Morton, 1988; Stone, 1983). This overuse combined with disregard of tension (because work termination might result in negative consequences) may lead to chronic muscular tension and subsequently pain. Rimehaug and Svebak (1987) have shown that high motivation and negative affect increase task-related EMG levels. This might explain why a number of epidemiological studies report the highest incidence of pain syndromes in workers who are under physical strain related to the affected body part but also report job dissatisfaction and other life stressors (Demjen & Bakal, 1986; Frymoyer 8~ Cats-Basil, 1987; Magora & Schwartz, 1973). In the case of chronic pain of acute onset, a predating vulnerability may be present that might have contributed to the acute episode and/or may now act unfavorably in promoting chronicity. For example, patients with amputations are much more likely to develop phantom limb pain when there was pain in the limb prior to amputation (Pasnau & Pfefferbaum, 1976). It is also possible that constant hyperactivity of muscles may be damaging to joints and disks close to these muscles. Andersson, Grtengren, and Nachemson (1977) have shown a high correlation of movement and posture related EMG-levels and disk pressure. Thus it is possible that high levels of muscle tension related to stressors may also exert pressure on the disk that may subsequently contribute to herniation.

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Conclusion3

Thus, a physiological diathesis to nociceptive stimulation may be related to a range of genetic factors and learning experiences. More research is needed to identify the mechanisms contributing to this vulnerability. Animal experiments would be especially useful to examine the role of various types of learning experiences and their role in the development of chronic pain syndromes. A final common pathway to chronicity may be the development of a response stereotypy, that is, a consistent pattern of physiological responses to stimulation that is specific for an individual and based on the diathesis acquired (Lacey & Lacey, 1958). A predisposition may be necessary for the development of chronic pain but may not be sufficient. Precipitating

Factors: Aversive External and/or Internal Stimuli

Definition

Aversive internal or external stimuli, usually labeled “stressors”, may act as precipitating factors in the development of chronic pain syndromes. Stress is an elusive concept. We use the term stress in accordance with Lazarus (1966) as resulting from the ongoing transaction of potentially aversive stimulation (stressors) and result of the individual’s appraisal and coping efforts. For the purpose of simplifying our discussion we will treat appraisal and coping processes in the next section although they are an integral part of our definition and discussion of the role of stress. Stress may originally be viewed as resulting from unconditioned stimuli that lead to a multitude of physiological and biochemical as well as psychological responses but may become associated with conditioned stimuli through learning processes. Acute onset pain

We will first focus on the evolution of chronic pain from an acute, for episode. In acute pain, many activities that are neutral or pleasurable may elicit or exacerbate pain and are thus experienced as aversive and avoided. Over time, more and more activities may be seen as eliciting or exacerbating pain and will be avoided. Fear of pain may become conditioned to an expanding number of situations. Avoided activities may involve simple motor behaviors, but also work, leisure, and sexual activity (Philips, 1987). In addition to the avoidance learning, pain may be exacerbated and maintained in these encounters with potentially pain-increasing situations due to the anxiety-related sympathetic activation and muscle tension increases that may occur in anticipation of pain and also example, injury-related

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as a consequence of pain. These increases in nociceptive excitability may be site-specific. For example, Devor and J&rig (1981) showed that there is an increase of alpha-adrenergic receptors in neuroma that may partially explain the increase in nociceptive excitability ‘of body parts affected by nerve injury. Over time, additional physiological changes occur due to the increasing inactivity and immobility related to the avoidance behavior. These physiological changes may be quite specific (e.g., immobilization of a finger or a leg), Symptom-specific response stereotypy may develop at the affected site, that is, a tendency of the person to react to stressful stimulation with hyperactivity or hypoactivity of the affected body part. The research by Traue and his colleagues (1986,1989) on muscle tension headache has demonstrated muscular hyperactivity of the trapezius muscle in a number of stressful situations. Our own research on chronic back pain and temporomandibular pain and dysfunction (Flor & Birbaumer, 1988; Flor, Turk, & Birbaumer, 1985) also shows that hyperreactivity to stressful stimulation and/or delayed return to baseline levels only at the uflected muscle group are characteristic for a large number of these chronic pain patients. Walker and Sandman (1977) have reported similar findings for patients suffering from rheumatoid arthritis and Dickson-Parnell and Zeichner (1988) for women suffering from premenstrual back pain. Thus, a direct effect of these learning processes on physiology occurs due to the increase in physiological activation that may be especially marked at the site of the injury that is already more excitable. The subsequent avoidance behaviors may be reinforced by significant others, but also by the successful avoidance of undesirable activities. The health care system may also play a role in this process by its emphasis on bed rest and time-out from work that may be appropriate in early stages of an acute problem but may be detrimental later on (Fordyce, Brockway, Bergman, & Spengler, 1986).

Pain unrelated to trauma

As has been suggested by Hagberg (1984), prolonged activity in a high tension producing body position without the possibility to reduce tension sufficiently may increase the probability for this system to overreact to stressful stimulation. This or some other physiological vulnerability may be the basis for the development of stress-related gradually developing pain such as in many cases of temporomandibular pain, certain types of back pain, or headaches. The acute increase in muscle tension and related vasoconstriction may be interpreted as an anticipated fight-flight response that may once have served adaptive purposes (Hollis, 1982). In another group of patients withdrawal reactions might be more dominant leading

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to depression and inactivity in response to pain (Henry & Stephens, 1981). Such maladaptive ways of coping will be discussed in more detail in the next sections.

Physiology of behaviorally

mediated pain responses

As noted in the previous section, pain episodes as well as other stressors may trigger a host of autonomic and musculoskeletal reactions, most notably sympathetic activation and elevated muscle tension levels. If stress or pain-related muscular contractions occur repeatedly or are sustained, mechanoreceptors will be activated. This information is transmitted to the spinal cord. If the stimulation exceeds a critical level efferent fibers such as the gamma-motorneurons may be activated as well as sympathetic nerve fibers that are connected with the smooth muscle of the blood vessels. These muscular and sympathetic reflexes lead to increases in muscle tension via the gamma motor system and to sympathetically mediated vasoconstriction (R.F. Schmidt, 1985). If the muscular contractions are of sufficient intensity, frequency, and duration, ischemia and hypoxia may develop in the affected muscle and lead to the release of algogenic substances such as bradykinin (Fields, 1987). Subsequently, chemosensitive nociceptors will be activated directly and the thresholds of mechanosensitive receptors will be lowered (Mense, 1986; Mense & Schmidt, 1974; Mense & Stahnke, 1983). The ensuing pain experience increases muscular hyperactivity and sympathetic activity and may thus lead to a vicious circZe (Mark, Victor, Neshed, & Wallin, 1985; Wiesenfeld-Hallein & Hallein, 1984). Moreover, nociceptive input may be enhanced through “overflow” from sympathetic neurons at the sympathetic ganglia and the spinal cord. An extended stimulation of the sympathetic nerve system will lead to the release of adrenaline and noradrenaline, substances that increase the sensitivity of chemo-nociceptors as well (Wall & Gutnick, 1974; WiesenfeldHallein & Hallein, 1984). For example, Morishima, Pedersen, and Finster (1978) reported significant increases in peripheral catecholamine levels (especially noradrenaline) and decreases in uterine blood flow during maternal stress. Longstanding muscular contractions may lead to destruction of muscle fibers, chronic hypoxia, a lack of ATP and phosphocreatinine (Henriksson & Bengtsson, 1988). In addition, the endogenous opioids play an important role during acute stress responses. Plasma endorphin levels increase dramatically during certain stress responses (Howlett et al., 1984). Acute stressors usually produce decreased sensitivity to painful stimuli, so called stress-induced analgesia (SIA). Grau, Hyson, Maier, Madden, and Barchas (1981) reported an initial non-opioid-mediated hypoalgesia to stress in laboratory animals when

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painful shocks are used (trials 5-20), then an increasing algesia and a second opioid-mediated hypoalgesic peak at trials 80-100 or more. This second peak also depends on the uncontrollability of the shock. Contxdlable shock does not appear to produce this second hypoalgesia. The second peak is also dependent on prior experience with the stressor. Thus, there appear to be two types of opioid stress-induced analgesia, One is a hormonal opioid SIA that depends on the pituitary-adrenal system, the other is a non-hormonal SIA (Watkins & Mayer, 1983). The hormonal type depends on more frequent stress exposure that is more shock trials than the non-hormonal one. Whereas the initial non-opioid hypoalgesia in stress situations does not depend on learning, the second opioid hypoalgesia does appear to depend on learning that the shock is inescapable (Maier, Dugan, Grau, & Hyson 1984; Maier & Keith, 1987). We will return to the issue of control in the section on cognitive processing, Based on Wagner’s (1981) model of memory processes in conditioning, Grau (1987) has suggested that memory activation plays a role in stressrelated hypoalgesia, specifically, that the memory of the aversive event elicits opiod release. If there is interference with the memory trace then there is no opioid hypoalgesia. Grau and his colleagues (Grau, 1987; Grau et al., 1981) have provided initial evidence suggesting that the release of endogenous opioids is much more related to the cognitive processing of aversive stimulation than its intensity and duration per se. In chronic pain patients pain episodes may present a constant stressor and the existence of a chronic pain syndrome may increase the perceived stressfulness of many otherwise non-stressful stimuli. For example, chronic pain patients often report negative consequences of chronic pain on mood, marital and sexual functioning, employment and financial status (Turner, Chancy, & Vitaliano, 1987; Turner & Romano, 1984). Feuerstein, Suit, and Houle (1985) reported more stressful life events as well as more problematic family and work relationships in chronic pain patients as compared to healthy controls. Recently, Flor and Birbaumer (1988) also reported increased daily hassles, more marital and work-related conflicts, less perceived social support and less problem solving abilities in chronic pain patients as compared to healthy controls. Andrasik et a1. (1982) also noted more stressful life events in chronic headache sufferers and Kearney, Wilson, and Haralambous (1987) found more maladaptive cognitions and more stress-related cognitions in chronic headache sufferers. Moreover, Flor et al. (1985) demonstrated that patients suffering from chronic back pain respond with increased paravertebral EMG levels to discussions of pain or stress episodes. Similar symptom-specific psychophysiological responses have been found in tension headache (Thompson & Adams, 1984) and temporomandibular pain patients (Flor & Turk, 1989; Mercuri, Olson, & Laskin, 1979).

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The uncontrollability aspect is likely to play a major role in intractable chronic pain states. It might thus be possible that the constant experience of pain and related stressors leads to a decrease in opioid availability at the relevant synapses. This overutilization of the opioid system may lead to a progressive lack of stress-related analgesia and a state of hyperalgesia. A lack of self-efficacy and of perceived control is characteristic for chronic pain patients (Dolce, 1987; Flor & Turk, 1987). It might be speculated that this lack of control over aversive stimulation could be a factor contributing to a reduced availability of opioids. These speculative assumptions, however, do need empirical validation. The important role of endogenous opioids in the modulation of pain has been amply documented (cf., Frederickson, 1988). There is evidence that in chronic pain the functions of the algogenic and endogenous analgesic systems are changed. For example, Guilbaud and her coworkers (Guilbaud, 1988; Guilbaud, Gantrob, & Peschinski, 1981) demonstrated that in arthritic rats neurons that are stimulated by nociceptive input had different physiological properties than the same neurons in healthy animals. Moreover, certain brain areas that usually do not respond to painful stimulation were activated in arthritic rats. These central mechanisms might change the way nociceptive stimuli are processed and might also be reflected in a less efficient endogenous analgesic system. Several authors (Almay, Johannson, v.Knorring, Terenius, & Wahlstrom, 1978; Almay, Johannson, v.Knorring, Sakurada, & Terenius, 1985; van Knorring & Wahlstrom, 1983) have reported lowered beta-endorphin levels in the CSF of chronic pain patients. Bandura, O’Leary, Barr-Taylor, Gauthier, and Gossard (1987) reported that increases in pain tolerance related to cognitive coping skills training are at least partially opioid-mediated. It is possible, for example, that prolonged stress-such as is the case with chronic pain that is accompanied by beta-endorphin releases - may subsequently contribute to a reduction of the efficacy of the beta-endorphinergic system and may thus increase susceptibility to pain. Moreover, the experience of low self-efficacy and loss of control that is prevalent in chronic pain patients might be related to the changes in endogenous opioid systems. Additionally, the excessive use of narcotic medication in chronic pain patients also alters the function of the endogenous opioid systems. The pain-relieving alkaloid, ergotamine, for example, has been implicated in endorphin-suppression after long-term use (Meltzer, 1987). Longitudinal studies following patients from an acute to a chronic pain state or assessing high risk populations (e,g., children of chronic pain patients) would be especially helpful and would permit us to decide to what extent these stress responses are a cause or a consequence of chronic pain. Little research is currently available that will allow us to draw conclusions, with any confidence, about the causal role of stress in chronic pain. JAW

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Precipitating

Responses: Inadequate Proprioception Ability

Perception of physiological

and Lack of Coping

processes and bodily symptoms

The reaction to stressful stimulation is determined (a) by the appraisal of the stimulation, that is, how threatening it is perceived to be, and (b) by the cognitive or behavioral efforts to meet environmental and internal demands, that is the degree of helplessness it induces (Lazarus, 1966). The perception and interpretation of physical symptoms and physiological processes is important in all psychophysiological disorders (Birbaumer, 1975; Pennebaker, 1982). The perception of bodily symptoms and stimuli leads to certain interpretations (conscious and subconscious) and serves as an impetus for action (Nerenz & Leventhal, 1983; Pennebaker & Epstein, 1983). In chronic illness, there is a special problem that patients often adhere to the acute disease model with which they are most familiar. Patients therefore continue to seek a tangible physical cause of the problem even if they have received evidence that the original injury has resolved. Moreover, patients may interpret pain symptoms as indicative of an underlying disease process that, if the pain persists, could signify progressive disease and they may do everything to avoid pain exacerbations, most often by resorting to inactivity. For example, in acute pain states bed rest is often prescribed to relieve pressure on the spine. Patients ascribe to a belief that any movement of the back may worsen their condition and may still maintain this belief in the chronic pain stage when their inaction is not only unnecessary but harmful (Philips, 1987). As Pennebaker, Gonder-Frederick, Cox, and Hooever (1985) showed, once cognitive structures (memories and meaning) about a disease are formed they become stable and are difficult to modify. Patients tend to avoid experiences that could invalidate their beliefs and they guide their behavior in accordance with these beliefs even in situations where the belief is no longer valid. Consequently, they do not receive corrective feedback. A.J.M. Schmidt and his coworkers (Peters, A.J.M. Schmidt, & Van den Hout, 1989; A.J.M. Schmidt, 1985; A.J.M. Schmidt & Brands, 1986) have presented a series of studies that show that chronic pain patients display less endurance in many different situations that may be related to a lack of adequate perception of physical symptoms (A.J.M. Schmidt, Gierlings, & Peters, 1989). In the case of musculoskeletal pain syndromes such as chronic low back pain this may actually exacerbate the problem due to disuse and ensuing deterioration of the muscles. Interpretation

Another

of physical symptoms important

contributing

factor to the maintenance

of chronic

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pain may be viewed in the misinterpretation of physical sensations as painful symptoms. For example, Anderson and Pennebaker (1980) reported that healthy subjects rated an ambiguous but affectively neutral vibrating sensation as painful or pleasant depending on the information they were provided about the nature of the stimulus (painful or pleasant). In fact, they insisted later after debriefing that the sensation they had reported was exactly what they had felt. Thus, it is quite possible that patients will interpret normally non-painful sensations as painful if they have learned to do so and may subsequently be reinforced for these pain expressions, at least within certain limits of nociceptive input intensity. For example, Whitehead (1980) and Ritchie (1973) demonstrated that patients suffering from irritable bowel syndrome report pain at very low levels of bowel distension compared to healthy controls. Whitehead (1980) suggested that physiological responses with a lower threshold for conscious perception might be more likely reinforced than those that are difficult to perceive. The perception of changes in muscle tension, is a better developed skill than visceral perception (Hefferline, 1958). Unfortunately, Whitehead did not differentiate the perception of ongoing physiological responses from the perception of physical symptoms, two processes that are not highly correlated (Pennebaker, 1982; Pennebaker 8z Epstein, 1983). It is possible that chronic pain patients become preoccupied with and overemphasize physical symptoms related to increases in muscle tension and interpret them as a painful stimulation although they may be less able than healthy controls to differentiate tension levels. Data reported by Flor and Birbaumer (1988) provide some support for the proposition that chronic pain patients have a tendency to overemphasize physical symptoms and to misjudge levels of muscle tension. These authors demonstrated that pain patients complain of a high level of physical symptoms and anxiety in a stressful laboratory situation, and are less able to discriminate muscle tension levels than healthy controls. This is especially likely in the case of patients with few organic findings who are “in need” of demonstrable signs to justify their pain complaints. Studies that induced high levels of muscle tension during a headache free state in patients suffering from headaches report that these patients signalled pain at a much lower level of tension than healthy controls (Borgeat, Hade, Elie, & Larouche, 1984). It is possible that preoccupation with painful stimuli and a high probability of reinforcement for pain reports in famikes of pain patients (Apley & Hale, 1973) have increased the probability with which they label symptoms as painful. However, it is not clear if this labeling of muscle tension as painful is related to altered local physiological processes or if patients are more likely to perceive any sensation as painful thus indicating a generalized lowering of pain perception threshold (Tunks, Crook, Norman, & Kalaher, 1988). This issue warrants more careful experimental investigation.

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Even in non-muscular pain states the interpretation of painful stimulation may be important. For example, Spiegel and Bloom (1983) reported that the pain severity ratings of cancer patients could be predicted by the use of analgesics, the putients’ affective state, but also the itzterpretution of thepuin. Patients who attributed their pain to a worsening of the underlying disease process experienced more pain despite the same level of disease progression as compared to patients with a more benign interpretation of the pain. Anticipation

of pain

In acute pain states induced in the laboratory, forewarning about the painful stimulation may reduce its aversive impact, especially if there is some form of control over the aversive stimulation (Averill, 1973). There is, however, also ample evidence that the explicit expectation of uncontrollable painful stimulation may make the following nociceptive input be perceived as more intense (Leventhal & Everhart, 1979). Thus, patients who have associated activity with pain may expect heightened levels of pain when they attempt to get involved in activity and then actually perceive higher levels of pain or avoid activity altogether. A.J.M. Schmidt (1985) and A.J.M. Schmidt and Brands (1986) have shown that patients suffering from chronic low back pain perform more poorly on a treadmill task and on the cold pressor test; however, the poor performance in the treadmill task did not appear to be related to reports of pain or physical exertion but rather to previous pain reports. Furthermore, performance in the cold pressor test could be best predicted by the patients’ belief in their ability to perform well on the task. The presence of pain may change the way individuals process painrelated and other information. For example, the presence of chronic pain may focus attention on all types of bodily signals. Chronic pain patients are known to complain about a multitude of bodily symptoms in addition to pain (A.J.M. Schmidt et al., 1989; Turk & Flor, 1987). Demjen and Bakal (1986) have shown that patients tend to become more preoccupied with their pain the longer the pain endures. The high scores of many chronic pain patients in hysteria and hypochondriasis scales of the MMPI might reflect this preoccupation with bodily processes as these scales include the preponderance of items related to somatic functioning (Bradley & van der Heide, 1984). Conversely, the expectation of pain reduction may already by itself reduce pain perception and avoidance. For example, Notterman, Schoenfield, and Bersh (1952) paired painful electric shock with a tone and measured heart rate in conditioning trials. They reported that subjects who were informed about the onset of extinction trials and those who

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could avoid shock showed faster extinction than uninformed subjects. Thus, expectation of pain reduction reduced avoidance independent of the actual event. Consequently, medication, avoidance of activity, bedrest may obtain additional reinforcing properties by the associated positive effects of the anticipation of pain reduction. State dependent learning

The expectation of painful stimulation may also be enhanced by the fact that patients tend to be more likely to rememberpain when they are in apain stare than when they are not (Eich, Reeves, Jaeger, & Graff-Radford, 1985; Linton & Gotestam, 1985). Thus they may selectively focus on stimuli that predict pain and become overavoidant. Moreover, images and thoughts of impending pain or exacerbations of pain instigate sympathetic activation and may themselves become stimuli for the activation of nociceptive input (c.f., Rachman & Lopatka, 1988). For example, Rimm and Litvak (1969) demonstrated that subjects exhibit physiological arousal when they only think about or imagine painful experiences. Flor et al. (1985) and Flor and Birbaumer (1988) noted that the mere discussion or imagination of painful events produces increases in heart rate, skin conductance, and frontalis EMG in all subjects, and very pronounced increases in EMG levels at the affected site of pain patients compared to healthy controls. Thus, activation of a memory of a painful or stressful event may elicit peripheral responses that are part of the propositional network of this event (Lang, 1979) and that may contribute to increases in pain perception. A study by Barber and Hahn (1964) provides additional evidence for this assumption. They showed that subjects’ self-reported discomfort and physiological responses (frontalis EMG, HR, SCR) were similar when they merely imagined taking part in a cold pressor test as compared to actually participating in it. In patients suffering from recurrent migraine headaches, Jamner and Tursky (1987) observed increases in skin conductance related to the processing of words describing a migraine headache. Controllability

There are many laboratory studies demonstrating that controllability of aversive stimulation reduces its impact considerably (for a review see Averill, 1973; Thompson, 1981). In chronic pain patients, a lack of personal control is typically perceived by the patient and likely related to the ongoing but unsuccessful efforts to control their pain. Furthermore, uncontrollability augments the perception of pain intensity (Miller, 1981). This relationship has been demonstrated in a variety of chronic pain syndromes. Brown and Nicassio (1987) showed that active coping is related

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to better, and passive coping is related to poorer adjustment in patients suffering from rheumatoid arthritis. Recently, Flor and Turk (1988) examined the relationship between general and situation specific pain-related thoughts, convictions of personal control, pain severity, and disability levels in chronic low back pain patients and rheumatoid arthritics. The general and situation specific convictions of uncontrollability and helplessness were more highly related to pain and disability than disease-related variables for both samples. The combination of both situation specific and general cognitive variables explained 32% and 60% of the variance in pain and disability, respectively. The addition of disease related variables improved the predictions only marginally (see also Smith, Follick, Ahern, & Adams, 1986). Self-eficacy

Closely related to the sense of control over aversive stimulation is the concept of self-efficacy. Self-efficacy denotes the conviction that one is able to display a certain required behavior in a given situation (Bandura, 1977) and has been proposed as a major mediator of therapeutic change. Dolce et al. (1986) and Litt (1988) reported that low self-efficacy ratings regarding pain control are related to low cold pressor pain tolerance, and they are better predictors of tolerance than pain levels. Several studies also obtained self-efficacy ratings from pain patients and related them to patients’ ability to control pain. For example, Manning and Wright (1983) obtained self-efficacy ratings from primipara concerning their ability to have a medication-free childbirth. These ratings were good predictors of medication use and time in labor without medication. Similarly, Council, Ahern, Follick, and Kline (1988) had patients rate their self-efficacy as well as expectancy of pain related to the performance of movement tasks. Patients’ performance levels were highly related to patients’ self-efficacy expectations that in turn appeared to be determined by patients’ expectancy of pain levels. In a laboratory study, Bandura et al. (1987) assessed self-efficacy ratings for pain tolerance and pain reduction in a cold pressor test in subjects who received cognitive skills training, subjects who received placebo medication, and control subjects. Injections of naloxone (an opiate antagonist) reduced the pain tolerance that had been substantially improved after cognitive coping skills training and also affected placebo analgesia but not the untreated control group. Nor did a saline injection (placebo) have any effect. In a subsequent experiment, Bandura, Cioffi, Taylor, and Broulliard (1988) induced high or low self-efficacy in their subjects. Subsequently, the subjects received either saline or naloxone and were exposed to an acute pain stimulus. The subjects who were low in

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self-efficacy and had received naloxone, showed a very low pain tolerance as compared to the low-self-efficacy subjects who had received saline and the non-efficacious subjects. Bandura et al. (1987, 1988) concluded that the physical mechanism by which self-efficacy influences pain perception may at least be partially mediated by the endogenous opioid system. This conclusion fits well with the data from Maier et al. (1984) who showed that the uncontrollability of the stressor elicits opioid-mediated hypoalgesia. Opiod release is closely related to psychological factors, especially a subject’s sense of control. Coping

It is our supposition that the pain-inducing processes described in the previous sections will be accelerated if a person has few resources to cope with stressful events and pain. The type of coping with stressful stimulation may be relevant for the development of specific chronic pain syndromes. One type of distinction among types of coping is to distinguish more uctive, aggressive encounters with stress from those that are more passive, leading to giving up and conservation-withdrawal (cf., Henry & Meehan, 1981). There may be differences in the type of coping between various chronic pain syndromes that might be related to the type of syndrome that is acquired because various coping styles have been related to several patterns of physiological and hormonal responses. For example, Traue et al. (1986) and Bischoff, Traue, and Zenz (1982) reported that patients suffering from muscle tension headache are much less expressive in their non-verbal communication than healthy controls. They suggest that they might have developed a style of coping with stress in the way of inhibiting the expression of emotions but at the same time displaying excessive muscular overactivity. This fits well with results reported by Martin and Nathan (1987) and Woods, Morgan, Day, Jefferson, and Harris (1984) who found a high prevalence of the type A behavior pattern in patients suffering from chronic headaches and also a higher frequency of headaches in subjects with high type A scores. It is possible that these patients respond to stress habitually with overactivity and frequent increases in muscle tension and sympathetic activation that may over time lead to the changes in nociceptive input described above. An alternative response pattern might be one of giving up, uGr~&zi~u~ und depression, leading to increased inactivity and immobility with increased tonic muscular tension, thus also affecting the muscular system (Lader, 1975). As suggested earlier, inactivity leads to increased focus on and preoccupation with the body and pain, per se, thus increasing the likelihood of misinterpretation and overemphasis of symptoms. Moreover, long periods of immobility will lead to muscular atrophy and reduction in the

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stabilizing function of many muscles. This process of deconditioning may then lead to degenerative changes in the muscles and joints or may accentuate pre-existing deficiencies (cf., Andersson et al., 1977). A solicitous spouse and/or well-meaning health care professional may further reinforce inactivity and thereby lead to still less physical movement and greater muscle deficiency.

MAINTAINING VARIABLES: THE ROLE OF LEARNING PROCESSES Throughout our presentation, we have emphasized the role of learning processes in the acquisition of a diathesis as well as the response to pain and stress. In this section we will discuss these processes in more detail as they apply to the maintenance of chronic pain behavior.

Instrumental

Learning

We have already mentioned the influential operant conditioning model of chronic pain presented by Fordyce (1976). Specifically, the operant conditioning model suggests that the maintenance of pain behaviors may occur through a process of reinforcement and, consequently, instrumental learning. The model does not directly concern itself with pain but rather the overt manifestations of pain and suffering (e.g., moaning). Because of the consequences of specific behavioral responses, it is proposed that pain behaviors may persist after the initial cause of the pain is resolved or greatly reduced. We have previously described how positive and negative reinforcement of pain behaviors as well as lack of reinforcement for well behaviors may contribute to the maintenance of pain behaviors. Linton et al. (1985) have elaborated on some points of the operant model. Specifically, they described that in escape learning, pain serves as a discriminative stimulus (SD) for actions that terminate pain such as lying down, changing the posture, or taking pain medication. As a consequence, the punishing stimulus (S-) is removed. In avoidance learning, the subject avoids the situation or rather does not approach it so that the noxious stimulus never occurs. For example, the patient may not even assume a posture that might cause pain. This process occurs later in the learning sequence when all the necessary associations have been made. Avoidance learning is particularly resistant to extinction. As SDS are often also conditioned stimuli (see later), there may be negative reinforcement due to fear reduction that may also motivate avoidance behavior. As a consequence of this avoidance disuse of body parts may occur because of the restricted

Psychobiology

of Pain

71

activity, muscle fibers shorten and lose elasticity. That may lead to pain when movement is attempted. When this pain is reported to the physician he or she may assume that the pain is related to the original injury. The operant model has proven to be of heuristic value in delineating treatment approaches for chronic pain. The exclusive focus on pain behaviors is, however, a limitation because the principles of operant conditioning also apply to covert processes and to physiological responses (Miltner, Larbig, & Braun, 1988). There is very little direct evidence for the instrumental learning view of pain in humans, although it has had great impact on the treatment of chronic pain patients. Numerous treatment studies showed that the operant approach to chronic pain is successful (Linton, 1986; Malone & Strube, 1988) though most were uncontrolled. Cairns and Pasino (1977) and Doleys, Cracker, and Patton (1982) showed that pain behaviors (specifically, inactivity) can be decreased and well behaviors (i.e., activity) can be increased by verbal reinforcement with or without feedback, and the setting of exercise quotas. A step in the direction of assessing the development and maintenance of pain behaviors was undertaken by Block, Kremer, and Gaylor (1980). These authors demonstrated that pain patients reported differential levels of pain behaviors in an experimental situation depending on whether they were observed by their spouse or ward clerks. Pain patients with nonsolicitous spouses reported more pain when a neutral observer was present than when the spouse was present. When solicitous spouses were present, pain patients reported more pain than in the neutral observer condition. Recently, Flor, Kerns, and Turk (1987) found that chronic pain patients reported more intense pain and less activity when they indicated their spouses were solicitous. The two later studies suggest that spouses can serve as discriminative stimuli for the display of pain behaviors by chronic pain patients, including their reports of pain intensity. In a laboratory investigation with acute pain stimuli, Linton and Gotestam (1985) showed that verbal reinforcement of pain reports led to altered reports of pain intensity despite constant nociceptive input. Wooley, Epps, and Blackwell (1975) had subjects perform the cold pressor test under two conditions: (a) with the experimenter close to the subject, wearing a white coat, providing verbal reinforcement and reassurance, and (b) the experimenter sat across the room in street clothes and subjects were not reinforced. The experimenters report that subjects in the non-reinforcement condition stayed in the experiment much longer and had a much longer tolerance time. Wooley and Blackwell (1975) also reported that when patients could distribute tokens for behaviors they wanted to encourage in other patients, they gave tokens mainly for caretaking i.e. reinforcing behaviors.

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Data that argue against the role of reinforcement of pain behaviors by compensation payments have, however, been reported by Peck, Fordyce, and Black (1976). They noted that litigation pending that involved a third party was not associated with more pain behaviors as compared to litigation that did not involve a third party. This might be related to the long temporal delay between the behavior and the consequence (Linton et al., 1985).

Respondent Conditioning An important learning process in the development and the maintenance of chronic pain states may be the respondent conditioning of fear of activity and subsequent avoidance of activity. The role of respondent conditioning in chronic pain has so far not received sufficient attention, although it might be a process that often occurs prior to instrumental learning (Brener, 1986). Moreover, although the role of respondent conditioning in the chronicity of acute pain states has at least been mentioned, the role of respondent factors in gradually developing pain states such as chronic headaches is completely unknown. Factors contributing to chronicity that have previously been conceptualized in terms of operant or cognitive variables may also be initiated and maintained by respondent conditioning. For example, in acute pain states it may be useful to reduce movement to further the healing process. Over time, however, anticipatory anxiety related to activity may develop and act as a conditioned stimulus (CS) for sympathetic activation (conditioned response, CR) that may be maintained after the original unconditioned stimulus (US, e.g., injury) and unconditioned response (UR, pain and sympathetic activation) have subsided (Lethem et al., 1983; Linton et al., 1985). Pain related to sustained muscle contractions might, however, also be conceptualized as a US in the case where no acute injury was present and sympathetic activation and tension increases might be viewed as UR that may elicit more pain, and conditioning might proceed in the same fashion as outlined above. Thus, although the original association between pain and pain-related stimuli results in anxiety regarding these stimuli, with time the expectation of pain related to activity may lead to avoidance of adaptive behaviors even if the nociceptive stimuli and the related sympathetic activation are no longer present (see Seligman & Johnston, 1973, on the role of expectation in learning processes). Sanders (1985) has pointed out that the classical conditioning of pain is of the Pavlovian-B conditioning type which may explain its persistence. In Pavlovian-B conditioning, the US is an aversive event as compared to Pavlovian A-type conditioning (pleasant stimuli; cf,, Grant, 1964). In B processes, the UR is usually less discrete, and very intense. Also, the CR is often more similar to the UR than with A processes (with regard to

Psychobiology of Pain

n

duration and mtensity). Also, B-type CRs are very resistant to extinction and this makes the persistence of the avoidance response more likely. Pain eliciting stimuli are often associated with prepwed US, such as human crying, facial expression of fear and disgust. ohman (1985) has demonstrated that responses to prepared stimuli showed much slower extinction than stimuli without such a genetic association. Non-occurrence of pain is a powerful reinforcer for reduction of activity and thus the original respondent conditioning may be completed by an instrumental learning process whereby the nociceptive stimuli and the associated responses need no longer be present for the avoidance behavior to occur. Thus, from a conditioning perspective, the patient may have learned to associate increases in pain with all kinds of stimuli that were originally associated with nociceptive stimulation (stimulus generalization). Sitting, walking, engaging in cognitively demanding work or social interaction, sexual activity, or even thoughts about these activities may increase anticipatory anxiety and concomitant physiological and biochemical changes (Philips, 1987). Subsequently, patients may display maladaptive responses to many stimuli and reduce the frequency of performance of many activities other than those that initially induced pain. The physical abnormalities often observed in chronic pain patients (such as distorted gait, decreased range of motion, muscular fatigue) may thus actually be secondury to changes initiated in behavior through learning. As the pain symptoms persist, more and more situations may elicit anxiety and anticipatory pain and depression because of the low rate of reinforcement obtained, when behavior is much reduced (cf., Lethem et al., 1983). Usage of medication may be based on the anticipation of pain and be viewed as an avoidance behavior. Excessive medication may in itself cause medication-induced pain (cf., Diener & Dichgans, 1988). Thus, expectations may lead to modified behavior that in turn may produce physical changes leading to still further physical abnormalities, particularly in the muscles and the joints. With chronic pain, the anticipation of suffering or prevention of suffering may be sufficient for the long-term maintenance of avoidance behaviors. None of these processes occur necessarily on a conscious level. Processing of respondent learning is possible without any awareness of S-R connections (Dixon, 1981). The respondent model also proposes that, among other mechanisms, increases in muscle tension and sympathetic activation and thus lowered nociceptive threshold may become a conditioned response and maintain a pain-tension cycle. These processes might be able to explain the often observed desynchrony of the three levels of pain (i.e., physiological, behavioral, verbal-subjective) in chronic pain patients (cf., Lang, 1979; Lethem et al., 1983). Thus, the original injury may have healed, but the patient still complains about pain and shows pain behaviors that may now be

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maintained by the avoidance-related inactivity and medication intake and no longer be associated with the original nociceptive stimulation. Lethem et al. (1983) suggested that the functional-organic distinction be dropped and instead they suggest that the patients be assessed with respect to desynchrony of the sensory and emotional component. Unfortunately this differentiation opens again the road for a dualistic conce$tualization. It might be more practical to assess desynchrony with respect to the three levels of pain behavior. It is important to note here that pain-related conditioned anxiety is usually not global but may only be elicited when specific environmental, social or visceral CSs are present. The conditioning processes described above and the subsequent avoidance behavior might also play a role in early learning and might be instrumental in eliciting pain responses in a variety of emotionally arousing situations. For example, Bischoff and Traue (1983) describe a case in which a headache patient who had been physically abused as a child subsequently developed anxiety and related increases in muscle tension in social situations he tended to avoid. Similarly, Domino and Haber (1987) reported an increased incidence of physical and sexual abuse in chronic pain patients. Unfortunately, there is no more than anecdotal data available. There is some experimental evidence for the role of classical conditioning in chronic pain states. Flor et al. (1985) showed that state anxiety levels and spinal immobility of chronic back pain patients tested in a demanding experimental situation were significantly positively correlated (r = S9, ~<.05) suggesting a positive relationship between anxiety and inactivity. Similarly, Flor and Birbaumer (1988) reported significant increases in state anxiety levels in chronic pain patients as compared to healthy controls when they anticipated the performance of a potentially pain-eliciting movement task. Dolce et al. (1986) showed that tolerance time of chronic pain patients was not related to current pain ratings but self-efficacy ratings, which may be understood as an indicator of expectations related to pain tolerance. Linton (1985) assessed the relationship between activity levels and expectations of pain. He was able to demonstrate that current pain levels could not predict activity levels whereas expectations of activity-related pain could. Pope, Rosen, Wilder, and Frymoyer (1980) examined the relationship between spinal mobility and pain tolerance in low back pain patients and reported a high positive correlation between the two variables. Moreover, low tolerance and low mobility were related to unfavorable long term outcome. This close relationship between avoidance behavior, anticipatory anxiety, and inactivity supports the assumptions of the respondent view. Instrumental and respondent learning are likely to interact in most chronic pain syndromes. The importance of respondent conditioning and avoidance learning in chronic pain states has so far not received sufficient consideration and should be a target for more research efforts.

Psychobiology

SUMMARY

75

of Pain

AND FUTURE

DIRECTIONS

We have described what we believe to be principal psychobiological interactions in chronic pain states. We have argued that, given a diathesis, psychological processes may play an important role in the evolution and maintenance of chronic pain. We described some preliminary evidence supporting our contention that chronic pain patients are more susceptible to stress and more likely to cope inadequately and misinterpret bodily symptoms than healthy controls. Moreover, the impact of chronic pain seems to be related to conscious and non-conscious appraisal of behavioral as well as cognitive coping with stressful stimulation. We have suggested that learning plays an important role in maintaining chronic pain be it by means of modeling, instrumental or respondent learning. These factors have to date only been inadequately addressed in research on chronic pain. Although we have witnessed a surge of psychological interventions for chronic pain there has been a lack of basic research that would permit us to know more about the way psychological factors operate in chronic pain. It is therefore of primary importance to concentrate on research delineating these mechanisms. The use of animal models of chronic pain and longitudinal studies in animals are clearly indicated. In addition, prospective longitudinal research in pain patients following the course from acute to subacute and chronic pain is important. Furthermore, research that focuses on children and adolescents with pain would be of great value as it would allow to follow the development of chronic pain. It is important to differentiate etiological and maintaining factors. For example, we showed that inadequate coping with stressful stimulation plays an important part in the development of musculoskeletal pain syndromes such as recurrent headaches whereas operant factors might be more powerful in injury-related pain problems. The relationship of pain and controllability may also differ according to the type of pain problem (cf., cancer-related pain versus recurrent headaches). It may also be important to identify subgroups of patients within different diagnostic categories that show a common pattern of coping. What are the implications of a psychobiological view for assessment and treatment of chronic pain? Turk and Rudy (1987) have proposed a multiaxial assessment of chronic pain. This is a first step in the direction of assessing and integrating psychological and physical findings to fully understand and evaluate the chronic pain patient. Based on the variables named above it would be worthwhile to assess the role of respondent, operant, and cognitive antecedents and consequences of pain on the somatic, psychological, as well as environmental level. Only the careful evaluation of the contribution of the relevant variables in a specific chronic pain syndrome will yield a more than just symptomatic treatment approach.

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We have enumerated a number of cognitive and behavioral factors involved in the processing of and coping with pain. Although most of the interactions we have discussed are speculative and the data supporting our assumptions are scarce, we have tried to integrate the disparate models and data in an effort to stimulate more comprehensive, integrated research efforts. Besides a lack of experimental research delineating the exact role of these variables in the perception of and responses to pain there has been a consistent failure to relate these factors to their physiological substrates. The research on the psychobiology of fear and anxiety (Eysenck, 1979; Gray, 1982) could serve as a modei for research on the psychobiology of pain. - This paper is dedicated to Prof. Dr. R.F. Schmidt, University of W&burg, whose physiological research served as a guideline and model for our own behavioral approach.

Acknowledgements

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