Health Psychology Of Pain Research Paper

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1. Basic Terms

Pain is an adaptive phenomenon that signals impending danger to the body. Pain can, however, also be maladaptive, for example in states of chronic pain, and thus can itself become a signiﬁcant disorder. Epidemiological studies show that 80 percent of the population experience recurrent pain, with more than 10 percent of the population being permanently disabled by it. Although pain has for a long time been viewed a purely sensory phenomenon or an epiphenomenon of a medical disorder, this view changed during the last 40 years of the twentieth century. It has been recognized that pain is a psychobiological experience, with emotional aspects being as important as sensory pain characteristics. Thus nociception, the physiological process of a noxious signal being transmitted from the periphery to the brain, has been diﬀerentiated from the experience of pain, which encompasses all aspects including psychological, social and cultural factors. The international Association for the Study of Pain (IASP) deﬁnition takes this shift from a biomedical to a biobehavioral or psychobiological perspective into account by characterizing pain as an ‘unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage’ (Merskey 1986). This deﬁnition was prompted by the fact that pain may often be experienced in the absence of identiﬁable objective pathology. A major change in the traditional view of pain was the gate control theory of pain proposed in Melzack and Wall (1965). More important than its physiological aspects, which have not all been conﬁrmed, was the conceptual model behind it. The gate control theory stated not only that pain could be modulated by both aﬀerent and eﬀerent factors at the level of the spinal cord, but also emphasized that pain has sensory–discriminative, motivational–emotional, and cognitive–evaluative components as well, and thus it assigns an important role to psychological factors. A core feature of this model is the integration of peripheral stimuli with psychological variables such as mood, attention, or cultural experience in the perception of pain. Thus, the gate control theory has been instrumental in abolishing the dichotomy of psychogenic versus somatogenic pain—psychological and physiological factors always interact in the production of the experience of pain and are not mutually exclusive causes of pain.

2. Classiﬁcation Of Pain

The common distinction between acute and chronic pain—referring to pain of at least three to six months duration and/or pain that exceeds the normal time for healing in the case of an acute injury—is useful, because chronic pain is often maladaptive and needs special attention. Whereas acute pain such as pain related to medical procedures or childbirth usually leads to anxiety and apprehension, chronic pain tends to be associated with helplessness, depression, and irritability as well as interference with family function, work, or social interaction (Gatchel and Turk 1999). In addition to the large number of workdays that are lost as a consequence of it, chronic pain is the leading cause of invalidity in the age under-50s group and causes enormous costs for the health care system (Melzack and Wall 1994).

The IASP classiﬁcation of pain is organized in ﬁve general categories: (a) the bodily system aﬀected, (b) time characteristics, (c) intensity of pain (d) duration of pain, and (e) its presumed etiology. This classiﬁcation lacks reliability especially in respect of the last characteristic. In addition, it neglects psychological factors that are only coded with respect to the presence of a psychiatric disorder or within the category ‘psychophysiological dysfunction.’ ICD-10 as well as DSM-IV still adhere to the distinction between psychogenic–somatogenic or physical vs. somatoform pain, which must be viewed as obsolete given the large number of research ﬁndings emphasizing the importance of psychological factors in any type of pain, both acute and chronic (Gatchel and Turk 1999).

The biopsychosocial model of pain views pain as a complex response that can be described on the verbal–subjective, the motor–behavioral and physiological levels. Pain can be based on nociceptive input, but nociception is not a prerequisite of the experience of pain, which can be an exclusively central phenomenon, but always has physiological antecedents and consequences (Flor et al. 1990). The multiaxial classiﬁcation of pain as proposed by Turk and his colleagues (cf. Turk and Rudy 1988) categorizes pain patients along both the somatic and the psychosocial dimensions. This classiﬁcation has yielded three subgroups of patients in the psychosocial domain characterized as adaptive copers, interpersonally distressed, and dysfunctional, with signiﬁcant diﬀerences in the course of the illness and response to treatment.

3. The Role Of Learning In Chronic Pain

Both associative and nonassociative learning processes as well as social learning have been found to be of fundamental signiﬁcance for the development of chronic pain. The repeated application of painful stimuli leads to reduced responsivity, i.e., habituation to the painful stimulation. In many states of chronic pain, sensitization rather than habituation occurs due to changes both at the level of the receptor and of the central nervous system (Woolf and Mannion 1999). Sensory information accelerates habituation and reduces activation caused by surprise, insecurity, and threat. This mechanism may underlie the eﬀects reported in a large number of studies that support the positive results of preparatory information prior to acutely painful procedures such as surgery or bone marrow aspiration.

The most inﬂuential model of psychological factors in chronic pain was Fordyce’s assumption that chronic pain can develop and be maintained due to operant conditioning of pain behaviors, i.e., overt expressions of pain. Fordyce (1976) postulated that acute pain behaviors such as limping or moaning may come under the control of external contingencies of reinforcement, and thus develop into a chronic pain problem. Positive reinforcement of pain behaviors (e.g., by attention and the expression of sympathy), negative reinforcement of pain behaviors (e.g., by attention and the expression of sympathy), negative reinforcement of pain behaviors (e.g., the reduction of pain through the intake of medication or by the cessation of activity) as well as a lack of reinforcement of healthy behaviors could provoke chronicity in the absence of nociceptive input. Thus, pain behaviors, originally elicited by nociceptive input, may, over time, occur in response to environmental contingencies. This model has generated much research, which has not only conﬁrmed the original assumptions made by Fordyce; it has also been shown that in addition to pain behaviors the subjective experience of pain, as well as physiological responses related to pain, are subject to reinforcement learning.

A special role has been assigned to the ‘signiﬁcant others’ of chronic pain patients, who have high reinforcement potential. When solicitous, i.e., painreinforcing, spouses were present, several studies found that the patients were more pain-sensitive during acute pain tests than when the spouses were absent. The patients with nonsolicitous spouses did not diﬀer whether the spouse was present or absent. These 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. Health care providers may also serve as discriminative cues inﬂuencing patients’ responses. Solicitous responses by signiﬁcant others can also lead to increased physiological pain responses in the patients, whereas the focusing on healthy behaviors by signiﬁcant others can have positive eﬀects on the pain experience.

Of equal importance is the operant conditioning related to the intake of pain medication. Patients are often told by their physicians or by well-meaning family members that they should not continue to take analgesic medication unless the pain increases to a point where it becomes intolerable (referred to as prn from the Latin, ‘take as needed’). When pain medication is taken at that stage, both pharmacological and behavioral factors can contribute to the development of the misuse of medication and, in severe cases, even drug dependence. If analgesic medication is taken only at peak pain levels, the eﬀect of the medication is less potent, and patients cycle between high and low levels of medication that facilitate the development of dependence. In addition, medication intake is negatively reinforcing, since the intake of medication ends an aversive state (pain). Subsequently, the pain-reducing behavior (use of analgesics) increases in frequency. Thus, both pharmacotherapists and behavioral psychologists recommend that analgesic medication should be taken not in a paincontingent but rather in a time-contingent fashion, adapted to the speciﬁc pain level of the patient and to the half-life of the drug.

The negative reinforcement of activity levels is an important process in the development of disability. A speciﬁc activity, for example walking, is performed until pain sets in, at which point the activity is interrupted and replaced by rest. Subsequently, the pain will be reduced. The reduction of an aversive state—pain—negatively reinforces the cessation of activity. As was the case with the intake of analgesic medication, the cessation of activity has to be made dependent on the amount of activity achieved—quotabased (e.g., number of stairs climbed, distance walked) rather than on the amount of pain. Thus, the painreinforcing quality of rest is eliminated. This formulation supports the strategy of encouraging patients to perform activities to meet a speciﬁc quota, and not until pain is perceived as overwhelming.

The respondent conditioning model postulates that numerous, formerly neutral, cues can be associated with the experience of pain and can—over time— themselves elicit responses that lead to an increased pain response, and can create the experience of pain in the absence of nociceptive input. To illustrate this process, the patient may have learned to associate increases in muscle tension with all kinds of stimuli that were originally associated with nociceptive stimulation. Thus, sitting, walking, bending, or even thoughts about these movements, may elicit anticipatory anxiety and an increase in muscle tension. This fear of movement or ‘kinesophobia’ has been discussed as an important factor in the maintenance and exacerbation of chronic pain. Subsequently, patients may display maladaptive responses to any number of stimuli and reduce the frequency of performance of many activities other than those that initially reduced pain. Thus, although the original association between injury and pain results in anxiety regarding movement, over time the anxiety may lead to increased muscle tension and pain even if the nociceptive stimuli are no longer present. In addition, stress situations can increase muscle tension levels and cause sympathetic activation and may, thus, reinforce this process.

Many patients report that an acute pain problem evolved into chronic pain at a time where personal stressors co-occurred with the pain. Stress situations may serve as additional unconditioned stimuli and also as conscious stimulus for muscle tension increases, increased sympathetic activation, and subsequently pain. Nonoccurrence of pain is a powerful reinforcer for reduction of movement. Thus, the original respondent conditioning may be complemented by an operant process, whereby the nociceptive stimuli need no longer be present for the avoidance behavior to occur. People who suﬀer from acute back pain, regardless of the cause, may adopt speciﬁc behaviors (e.g., limping) to avoid pain and they may never obtain ‘corrective feedback’ because they fail to perform more natural movements. Reduction in physical activity may subsequently result in muscle atrophy and increased disability. In this manner, the physical abnormalities proposed by biomechanical models of pain may actually be secondary to changes in behavior initiated through learning. Chronic pain patients tend to focus their attention on impending pain and subsequently avoid many types of activity, thus fostering the development of disability and depression. The release of endogenous opioids—the body’s own analgesic system—may also be inﬂuenced by respondent conditioning as well as brain responses related to the experience of pain. Moreover, fear of pain and subsequent avoidance of activity is one of the best predictors of subsequent chronicity (Asmundson et al. 1999).

Response acquisition through the observation of others and modeling is an essential mechanism of learning new patterns of behavior. Children acquire attitudes about health and health care, and the perception and interpretation of symptoms and physiological processes from their parents and their social environment. They also learn appropriate responses to injury and disease, and thus may be more or less likely to ignore or over-respond to normal bodily sensations they experience. The culturally-acquired perception and interpretation of symptoms determines how people deal with illness; the sight of others in pain is an event that captures attention and may have survival value, may help to avoid experiencing more pain and help to learn what to do about acute pain. Modeling probably plays a part in the phenomenon of ‘pain-prone families’ families with a signiﬁcantly elevated occurrence of pain problems (Whitehead et al. 1994). It was, for example, reported that children show the same pain syndromes as their parents currently have, rather than the pain problems their parents had in their own childhood. The large cultural variations in pain expression are also import- ant. In common clinical practice, the acquisition or extinction of pain-related behavior by means of modeling has received little attention. However, there are occasional indications for the role of modeling in treating pain problems in children in burn units and in the treatment of postoperative pain.

Despite the great deal of data available on the modiﬁcation of experimentally induced pain behavior by means of modeling in normal (healthy) subjects, there are few experimental results concerning chronic pain patients. Nor are there any longitudinal studies of the development of pain syndromes in ‘pain-prone families.’ Further investigation is necessary for the evidence of modeling as a factor in the development of chronic pain disorders.

4. Cognitive Factors And Pain

Cognitive–behavioral models of chronic pain emphasize that the evaluation of the pain experience by the patient greatly determines the amount of pain that is experienced as well as its negative consequences (Turk et al. 1983). General assumptions that characterize the cognitive–behavioral perspective are: (a) people are active processors of information, not passive reactors; (b) thoughts (e.g., appraisals, expectancies) can elicit or modify mood, aﬀect physiological processes, inﬂuence the environment, and serve as impetus for behavior. Conversely, mood, physiology, environmental factors, and behavior can inﬂuence thought processes; (c) behavior is reciprocally determined by the person and by environmental factors; (d) people can learn more adaptive ways of thinking, feeling, and behaving; and (e) people are capable and should be involved as active agents in change of maladaptive thoughts, feelings, and behaviors.

From the cognitive–behavioral perspective, people suﬀering from chronic pain are viewed as having negative expectations about their own ability to control certain motor skills such as performing speciﬁc physical activities (e.g., climbing stairs, lifting objects) that are attributed to one overwhelming factor, namely, a chronic pain syndrome. Moreover, chronic pain patients tend to believe that they have a limited ability to exert any control over their pain. Such negative, maladaptive appraisals about their situation and personal eﬃcacy may reinforce the experience of demoralization, inactivity, and overreaction to nociceptive stimulation.

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

Pain, when interpreted as signifying ongoing tissue damage or a progressive disease, seems to produce considerably more suﬀering and behavioral dysfunction than if it is viewed as being the result of a stable problem that is expected to improve. A number of studies using experimental pain stimuli demonstrated that the conviction of personal control can ameliorate the experience of experimentally-induced nociception. Moreover, the type of thoughts employed during exposure to painful stimulation has been related to pain tolerance and pain intensity ratings. Catastrophizing thoughts have been associated with lower pain tolerance and higher ratings of pain intensity. In contrast, coping thoughts have been related to higher pain tolerance and lower pain intensity ratings.

Certain beliefs may lead to maladaptive coping, increased suﬀering, and greater disability. Patients who believe their pain is likely to persist may be passive in their coping eﬀorts and fail to make use of available strategies, even when in their repertoire, to cope with pain. Patients who consider their pain to be an ‘unexplainable mystery,’ may negatively evaluate their own ability to control or decrease pain, and are less likely to rate their coping strategies as eﬀective in controlling and decreasing pain.

Once beliefs and expectancies (cognitive schemata) about a disease are formed they become stable and very diﬃcult to modify. Patients tend to avoid experiences that could invalidate their beliefs, and they adapt their behavior in accordance with these beliefs, even in situations where the belief is no longer valid (no corrective feedback is received to discredit this belief). For example, feeling muscular pain following activity may be caused by lack of muscle strength and general deconditioning and not by additional tissue damage.

Self-regulation of pain and its impact depends upon a person’s speciﬁc ways of dealing with pain, adjusting to pain, and reducing or minimizing pain and distress caused by pain—their coping strategies. Coping is assumed to be manifested by spontaneously-employed purposeful and intentional acts, and it can be assessed in terms of overt and covert behaviors. Overt, behavioral coping strategies include rest, medication, and use of relaxation. Covert coping strategies include various means of distracting oneself from pain, reassuring oneself that the pain will diminish, seeking information, and problem solving. Studies have found active coping strategies (eﬀorts to function in spite of pain, or to distract oneself from pain such as activity, or ignoring it) to be associated with adaptive functioning; and passive coping strategies (depending on others for help in pain control and restricted activities) to be related to greater pain and depression. However, beyond this there is no evidence supporting the greater eﬀectiveness of one active coping strategy compared to any other (Fernandez and Turk 1989). Speciﬁc coping strategies need not always be adaptive or maladaptive. It seems more likely that diﬀerent strategies will be more eﬀective than others for some people at some times, but not necessarily for all people all of the time, or even the same person at diﬀerent times.

5. Pain And Aﬀective Factors

The aﬀective factors associated with pain include many diﬀerent emotions, but they are primarily negative in quality. Anxiety and depression have received the greatest amount of attention in chronic pain patients; however, anger has recently received considerable interest as an important emotion in chronic pain patients. Research suggests that from 40 to 50 percent of chronic pain patients suﬀer from depression (Romano and Turner 1985). There have been extensive and fruitless debates concerning the causal relationship between depression and pain. In the majority of cases, depression appears to be the patients’ reaction to their plight. The presence of depression is closely related to the feelings of loss of control and helplessness often associated with pain.

Several investigators have also found a close association between fear of pain and dysfunctional coping. In addition, high comorbidity between anxiety disorders and pain seems to be present. Muscular hyper reactivity to stress seems to be closely associated with fear of pain.

Anger has been widely observed in individuals with chronic pain. The internalization of angry feelings seems to be strongly related to measures of pain intensity, perceived interference, and reported frequency of pain behaviors. Anger and hostility are closely associated with pain in persons with spinal cord injuries. Frustrations related to persistence of symptoms, limited information on etiology, and repeated treatment failures along with anger toward employers, the insurance, the health care system, family members, and themselves, also contributed to the general dysphoric mood of these patients. The impact of anger and frustration on exacerbation of pain and treatment acceptance has not received adequate attention. It would be reasonable to expect that the presence of anger may serve as an aggravating factor, associated with increasing autonomic arousal, and having the eﬀect of blocking motivation and acceptance of treatment oriented toward rehabilitation and disability management rather than cure, which are often the only treatments available for chronic pain.

6. Biobehavioral Perspective

A biobehavioral perspective of chronic pain needs to consider the factors discussed above and their mutual interrelationships in the explanation of chronic pain. The existence of a physiological disposition or diathesis is one important component. This predisposition is related to a reduced threshold for nociceptive stimulation and can be determined by genetic factors or acquired through early learning experiences. For example, Mogil (1999) showed that large genetic variations in individual pain sensitivity exist. Very impressive evidence for the role of early traumatic experience comes from the work of Anand et al. (1999), who showed that minor noxious experience in neonate rats leads to dramatic alterations (sensitization) in nociceptive processing in the adult organism. A further component of the biobehavioral model is a response stereotype of a particular bodily system, such as exaggerated muscular responses of the lower back muscle to stress and pain that is based both on the diathesis and on aversive experiences present at the time of the development of the response. These aversive stimuli may include personal or work stress or problematic occupational conditions and will lead not only to painful responses but also to avoidance behaviors and associated maladaptive cognitive and aﬀective processes. The cognitive evaluation of these external or internal stimuli is of great importance in the pain response, as discussed above.

7. Memory For Pain

An important maintaining factor in this chronicity process is the development of pain memories. These pain-related memories may be explicit or implicit and may subsequently guide the patient’s experience and behaviors (Erskine et al. 1990). For example, pain patients have a tendency to remember preferentially negative and pain-related life events and show a deﬁcit in the retrieval of positive memories. The experience of chronic pain also leads to the development of somatosensory pain memories for example, an expanded representation of the aﬀected body part in the primary somatosensory cortex. This expanded cortical representation is accompanied by increased sensitivity to both painful and nonpainful stimuli, and may be further enhanced by learning processes or attention to painful stimulation. A dramatic example of a learned memory for pain has been found in phantom limb pain patients (Flor et al. 1995). In upper extremity amputees, the magnitude of the phantom limb pain was found to be proportional to the amount of reorganization in the primary somatosensory cortex, namely, the shift of the cortical mouth representation into the area where the amputated limb was formerly represented. The brain obviously maintains a memory of the former input to the deaﬀerented area. Subsequently, stimulation stemming from areas adjacent to the deaﬀerented zone elicit sensations and pain in the now absent limb. Phantom sensations and cortical reorganization are absent in congenital amputees. The focus of the biobehavioral perspective is thus on the patient and not just on the symptoms or the underlying pathology. This focus also requires that the treatment of the patients be tailored not only to medical factors, but that it incorporates psychosocial variables that may often be predominant in states of chronic pain.

8. Future Perspectives

At the end of the twentieth century, there has been an enormous increase of research in the neurosciences, where the mutual interactions of molecular and genetic as well as neuronal and behavioral variables have begun to be examined. This integration of the psychosocial and biomedical perspective is much needed and will bring substantial advances in our understanding of the phenomenon of pain. A further important development is the recent ﬁnding in neuroscience that the adult brain is enormously plastic and that learning processes as well as training measures have great impact on these plastic changes (Recanzone 2000). This opens the door for new approaches to treatment. It will also aid in delineating and eliminating the factors that lead to resistance to the treatment of chronic pain syndromes.

Bibliography:

Anand K J, Coskun V, Thrivikraman K V, Nemeroﬀ C B, Plotsky P M 1999 Long-term behavioral eﬀects of repetitive pain in neonatal rat pups. Physiol. Beha . 66(4): 627–37
Asmundson G J, Norton P J, Norton G R 1999 Beyond pain: The role of fear and avoidance in chronicity. Clinical Psychology Review 19: 97–119
Erskine A, Morley S, Pearce S 1990 Memory for pain: A review. Pain 41(3): 255–65
Fernandez E, Turk D C 1989 The utility of cognitive coping strategies for altering pain perception: A meta-analysis. Pain 38(2): 123–35
Flor H, Birbaumer N, Turk D C 1990 The psychobiology of pain. Advances in Beha Res Ther. 12(2): 47–84
Flor H, Elbert T, Wienbruch C, Pantev C, Knecht S, Birbaumer N, Larbig W, Taub E 1995 Phantom limb pain as a perceptual correlate of cortical reorganization—following arm amputation. Nature 375: 482–4
Fordyce, W E 1976 Behavioral Methods for Chronic Pain and Illness. Mosby, St. Louis, MO
Gatchel R J, Turk D C 1999 Psychosocial Factors in Pain: Critical Perspectives. Guilford Press, New York
Melzack R A, Wall P D 1965 Pain mechanisms: A new theory. Science 150: 3699–709
Melzack R A, Wall P D (eds.) 1994 The Textbook of Pain, 3rd edn. Churchill Livingstone, Edinburgh, UK
Merskey H 1986 Classiﬁcation of chronic pain: Descriptions of chronic pain syndromes and deﬁnitions of pain terms. Pain 3: 1–225
Mogil J S 1999 The genetic mediation of individual diﬀerences in sensitivity to pain and its inhibition. Proceedings of the National Academy of Sciences of the United States of America 96(14): 7744–51
Recanzone G 2000 Cerebral cortex plasticity: Perception and skill acquisition. In: Gazzaniga M S (ed.) The New Cognitive Neurosciences. MIT Press, Boston, MA
Romano J M, Turner J A 1985 Chronic pain and depression: Does the evidence support a relationship? Psychology Bulletin 97(1): 18–34
Turk D C, Meichenbaum D, Genest M 1983 Pain and Behavioral Medicine: A Cognitive–Behavioral Perspecti e. Guilford Press, New York
Turk D C, Rudy T E 1988 Toward an empirically-derived taxonomy of chronic pain patients: integration of psychological assessment data. Journal of Consulting and Clinical Psychology 56: 233–8
Whitehead W E, Crowell M D, Heller B R, Robinson J C, Schuster M M, Horn S 1994 Modeling and reinforcement of the sick role during childhood predicts adult illness behavior. Psychosomatic Medicine 56: 541–50
Woolf C J, Mannion R J 1999 Neuropathic pain: Aetiology, symptoms, mechanisms, and management. Lancet 353: 1959–64