INTRODUCTION Pain is the most pervasive and universal form of human distress and often contributes to dramatic reductions

in the quality of life (Hadjistavropoulos, T. & Craig, K. D., 2004, p.1). According to the International Association for the Study of Pain, pain is an unpleasant sensory and emotional experience associated with actual and potential tissue damage, or described in terms of such damage, or both.( International Association for the Study of Pain, 1986; cf : Cole B.E., 2002). This definition emphasizes the subjective and psychological nature of pain and appropriately avoids making the authenticity of pain contingent on an externally verifiable stimulus. Further Price (1999) also proposes that pain should be understood as a somatic perception involving a bodily sensation with qualities similar to those reported during tissue-damaging stimulation, an experienced threat associated with this sensation, and a feeling of unpleasantness or other negative emotions based on the experienced threat(Cole .B.E.,2002). Pain is primarily a psychological phenomenon rather than a physiological phenomenon as it represents a perceptual process associated with conscious awareness, selective abstraction, ascribed meaning, appraisal, and learning (Melzack & Casey, 1968; cf: Hadjistavropoulos, T.& Craig, K.D., 2004,p.1). Further, although it requires central integration and modulation of a number of afferent and central processes (i.e., sending messages toward the central nervous system and interacting with higher components of the central nervous system) and efferent processes (i.e., sending messages away from higher centers in the central nervous system and toward muscle or gland),emotional and motivational states are also central to understanding its nature (Price, 2000;cf: Hadjistavropoulos, T.,&Craig, K. D., 2004. p.2). Therefore, a unified theory of pain must integrate the understandings of advances in biological sciences (molecular biology, genetics, neuro-physiology, pharmacological sciences, etc.) with the product of work in the behavioral and social sciences, as well as the humanities, because pain cannot be understood solely at the level of gene expression, neuronal firing, and brain circuitry (Hadjistavropoulos, T.,& Craig, K. D., 2004. p.2). The field of psychology is central in the study, assessment, and management of pain because pain being a complex subjective phenomenon that is uniquely experienced by each individual, the psychological issues such as knowledge about idiosyncratic beliefs, appraisal and coping repertoires will be an essential component for optimal treatment planning and delivery and for evaluating treatment effectiveness. Thus, it is not unexpected that at least 2 of the 10 most influential clinicians and researchers in the field of pain (as assessed by survey of a random sample of members of the International Association for the Study of Pain [IASP]) are psychologists (Asmundson, Hadjistavropoulos, & Antonishyn, 2001;cf: Hadjistavropoulos .T.,& Craig K.D.,2004). Moreover ,the role of the psychologist in an interdisciplinary pain management team includes providing evidence-based psychological therapy to improve the patients ability to cope with pain and the interpersonal stresses and problems arising as a result of pain; providing education to other team members about the psychological needs and problems of pain patients;assessing psychological parameters and social/environmental factors that affect the patients pain experience and treatment outcome ; researching pain management and improving effective communication between patients and healthcare provide (Caris .H.F.,2002). As the role of psychological factors in chronic pain (Gamsa, 1994; Adams et al, 1994; Klaber-Moffett and Richardson, 1995; cf: Adams .N., Ravey .J.& Taylor.D.,1996) is well established, a number of psychological models have been proposed to explain the aetiology and perpetuation of chronic pain. Further,the various psychological treatment approaches have also been based on these models ( Adams .N., Ravey .J.& Taylor.D.,1996). Each has its own strengths and weaknesses and Gamsa (1994) has pointed out that none has been shown superior to the others (Adams .N., Ravey .J.& Taylor.D.,1996).

PSYCHOLOGICAL MODELS/THEORIES Early Theories of Pain The psychological and psychiatric aspects of pain had been infrequently noted by modern writers as early as 1768 (Innes S.I.,2005). By the second half of the 19th Century, however, pain was considered sensorial and organic causes were offered to explain all pains, even those without an obvious basis in tissue damage or organic disease. The belief that all pain was a direct result of tissue damage was firmly entrenched by the early 20th Century (Bonica J.J.,1983 ;cf : Innes S.I.,2005). One of them was Descartess (1644/1985) early mechanistic conceptions of pain which resulted in the biomedical specificity theory sometimes referred to as the alarm bell or push button theory (Melzack, 1973), because of its apparent simplicity (Hadjistavropoulos, T. & Craig, K. D., 2004. P.2). The Specificity theory proposed that injury activates specific pain receptors and fibers, which, in turn, project pain impulses through a spinal pain pathway to a pain center in the brain i.e., it maintains that free nerve endings are pain receptors which generate pain impulses that are carried by A-delta and C-fibers in peripheral nerves and by the lateral spinothalamic tract in the spinal cord to a pain center in the thalamus.( Coffey,,G.H.& Mahon.M.V.,1982) The psychological experience of pain, therefore, was virtually equated with peripheral injury. In the 1950s, there was no room for psychological contributions to pain, such as attention, past experience, anxiety, depression, and the meaning of the situation. Instead, pain experience was held to be proportional to peripheral injury or pathology ( Melzack, R. & Katz, J., 2004,p.14). This theory, however, does not explain the inhibition or exaggeration of pain by emotion or the continued presence of pain after surgery.( Coffey,G.H.& Mahon.M.V.,1982). Patients suffering from pain without a pathophysiological basis or signs often were considered crocks (Melzack, 1993; cf : Hadjistavropoulos .T.,& Craig K.D.,2004). The major opponent to specificity was labeled as pattern theory, but there were several different pattern theories (Goldscheider ,1894; Livingston,1943; Noordenbos ,1959,etc )and they were generally vague and inadequate ( Melzack & Wall, 1996;cf: Melzack R & Katz J., 2004,p.15). The pattern theory is based upon the belief that stimulus intensity and central summation are the critical determinants of pain (Melzack R & Wall P.D.,1965; Indeck W & Printz A,1975; cf : Coffey,,G.H.& Mahon.M.V.,1982 ). Related to theories of central summation is the theory that a specialized input controlling system normally prevents summation from occurring, and that destruction of this system leads to pathological pain states. This theory proposes the existence of a rapidly conducting fiber system which inhibits synaptic transmission in a more slowly conducting fiber system that carries the signal for pain. Under pathological conditions, the slowly conducting system establishes dominance over the fast with the result of slow, diffuse, burning pain or hyperalgesia. (Coffey,,G.H.& Mahon.M.V.,1982). Although seen in retrospect, pattern theories gradually evolved and set the stage for the gate control theory, none of these theories was there an explicit role for the brain other than as a passive receiver of messages. Further, this theory has been challenged because it does not explain the existence of specific end organs .However, the successive theoretical concepts moved the field in the right direction: into the spinal cord and away from the periphery as the exclusive answer to pain ,thus making its way up towards the brain. The first theory to integrate physiological and psychological mechanisms of pain within the context of a single model is the Gate Control theory. Melzack and Wall (1965) proposed that a hypothetical gating mechanism within the dorsal horn of the spinal cord is responsible for allowing or disallowing the passage of ascending nociceptive information from the periphery to the brain. These essential elements are as follows: The gating mechanism is influenced by the relative degree of excitatory activity in the spinal cord transmission cells, with excitation along the large-diameter, myelinated fibers closing the gate and along the small-diameter, unmyelinated fibers opening the gate.

Descending transmissions (i.e., from the brain to the gating mechanism) regarding current cognition and affective state also influence the gating mechanism (suggesting the importance of higher level brain activities and processes). The summation of information traveling along the different types of ascending fibers from the periphery with that traveling on descending fibers from the brain determines whether the gate is open or closed and,as such, influences the perception of pain .

Melzack and Casey (1968) further proposed that three different neural networks (i.e., sensory-discriminative, motivational-affective, and cognitive-evaluative) influence the modulation of sensory input. They also recognized that processing of input could occur in parallel, at least at the sensory and affective level. This revised model allowed for perceptual information regarding the location, magnitude, and spatiotemporal properties of the noxious stimulus, motivational tendency toward escape or attack, and cognitive information based on analysis of multimodal information, past experience, and probability of outcome of different response strategies ( Asmundson G.J.G.,& Wright K.D., 2004,pp 40).Therefore the experience of pain came to be viewed as a combination of both pathophysiology and psychological factors (Asmundson G.J.G.,& Wright K.D., 2004,pp 40). Clinical Applications Based on the gate control theory, counter irritation or physical stimulation can be used to reduce the pain, as increasing pain by increasing stimulation in one region is a way to get the gate to close ,thereby reducing the perception of pain(Melzack & Wall,1982).All of the physical stimulation methods to control pain are based on this principle. 1) The transcutaneous electrical nerve stimulation (TENS) technique of pain reduction involves placing electrodes on the skin and administering continuos electrical stimulation (Melzack & Wall,1982).Patients wear a small portable unit that attaches the electrodes to the skin;the degree of stimulation can be increased or decreased depending on the need.The stimulation does not hurt and typically leads to a feeling of numbness in the area which can be effective in reducing pain for sonme chronic conditions,such as phantom limb pain,arthritis, as well as pain following surgery. 2) Acupuncture is a technique in which needles are inserted at specific points on the skin , to control the pain. The technique is based on the idea that a persons health is dependent on the balance of energy flowing through the 14 channels of energy; and imbalances in them are corrected by inserting and twirling the needles.It is used to treat a variety of common health problems like nausea caused by chemotherapy and pregnancy, pain following dental surgery, painful menustruation , tennis elbow, low back and headache pain and carpel tunnel syndrome (Brattberg 1983;Helms,1987; Richardson & Vincent,1986) as well as pain during surgery in some cases(Melzack & Wall,1982). 3) Massage Therapy is a technique in which npeople receive deep tissue manipulation by a trained therapist.A number of studies by Field (1998) shows that massage therapy can reduce pain.In one of the studies by Field, it was found that patients with chronic back pain in the massage therapy group showed signioficantly less pain and anxiety,lower levels of depression, and even had greater range of motion in their backs compared to the control group.Similar studies suggests that massage can be effective in reducing the pain of childbirth, postsurgery pain and arthritis pain. Psychodynamic Theories Merskey (1998) observed that psychological explanations about motives for complaints about pain and psychodynamic theories gradually became popular during the early and middle parts of the 20th century (e.g., Ellman, Savage, Wittkower, & Rodger, 1942; Scott, 1948;cf : Hadjistavropoulos .T.,& Craig K.D.,2004). The psychodynamic model can be considered to be among the first to posit a central role for psychological factors in pain ( Merskey & Spear, 1967), albeit

with an emphasis on persistent (or chronic) rather than acute presentations (Asmundson G.J.G.,& Wright K.D., 2004,pp 37).The various psychodynamic models were similar in that they shift focus from physical pathology by conceptualizing persistent pain as an expression of emotional conflict (Asmundson G.J.G.,& Wright K.D., 2004,pp 38). The theory underlying these models is that emotional factors may generate and perpetuate chronic pain (Engel, 1959). The psychosocial variables which have been examined for their aetiological significance in chronic pain include personality factors such as depression (Bradley et al, 1993; Klapow et al, 1993; Ahles et al, 1987), hypochondriasis (Pilowsky, 1970), anxiety and obsessionality (Harper and Steger, 1978; Collet et al, 1986) and family dynamics (France et al, 1986)(cf : Adams .N., Ravey .J.& Taylor.D.,1996). According to Freud (Breuer & Freud, 18931895/1957) persistent pain was maintained by an emotional loss or conflict, most often at the unconscious level. Central to Freuds model was the process of conversion, or expressing emotional pain (i.e., the unresolved conflict) by converting it into physical symptoms that were a symbolic and more tolerable expression of the underlying emotional issues. Freud believed that the somatic expression of pain would subside with resolution of the emotional issues. These ideas have been subsequently modified and adapted by other theorists working within the framework of the psycho-dynamic tradition (Asmundson G.J.G. & Wright K.D., 2004,pp 38). In 1959 Engel introduced the concepts of psychogenic pain and the pain-prone personality to further explain the nature of persistent pain. It is pain in the absence of identifiable physical pathology that has, since Engels (1959) contribution, been referred to by many as psychogenic, or of psychological origin. The key elements of Engels position were that (a) persistent pain can, but need not, have a basis in physical pathology, and (b) in some people, it is a psychological phenomenon that serves a self-protective function. Further Engel framed his model from a developmental perspective in which a person amasses a large set of experiences wherein pain is associated with, and derives meaning from, the context in which it has occurred.( Asmundson G.J.G. & Wright K.D., 2004,pp 38) With regard to pain prone personality, Engel (1959) suggested that those with psychiatric conditions, as described by diagnostic nomenclature of the day (e.g., DSMI provided for the possibilities of hysteria, major depression, hypochondriasis, or paranoid schizophrenia), were particularly prone to experience persistent pain. Amendments to Engels model, such as Blumer and Heil-broons (1982) position on chronic pain as a variant of major depressive disorder, or masked depression, added depressed affect, alexithymia, family history of depression and chronic pain, and discrete biological markers (e.g., response to antidepressants) to the list of contributors to the pain-prone personality (Asmundson G.J.G. & Wright K.D., 2004,pp 38-39). It is questionable, however, whether the presence of psychiatric morbidity makes one more likely to use pain as an unconscious defense mechanism and, thereby, more prone to persistent pain (see, e.g., the July 1982 issue of The Journal of Nervous and Mental Disease, and Large, 1986;cf: Asmundson G.J.G. & Wright K.D., 2004,pp 38-39) However, using Roths (2000) analogy of the double-edgedsword, it is noteworthy that there are lingering and unwanted scars of this psychodynamic thrust. The early investigation of psychiatric patients with pain had led to the erroneous conclusion that physical and psychological factors in pain were mutually exclusive and that pain is either physical or psychological (IASP Ad Hoc Subcommittee for Psychology Curriculum, 1997). Persistent pain with no identifiable causes was frequently labeled as psychogenic, a regrettable construct because it perpetuates mind/body dualistic thinking (Liebeskind & Paul, 1977) and fails to recognize that biological mechanisms are integral to all psychological phenomena, including pain. These assumptions can (and still often do) have a negative impact on opinions and general treatment of people who suffer from persistent pain conditions. Clinical Application It is the final treatment option for those who have not responded to other forms of psychological intervention or have not maintained treatment gains (Grzesiak, Ury, & Dworkin, 1996). It has been speculated that this form of treatment is appropriate for those individuals who have had early experiences (e.g., trauma, loss, abandonment) that lay a foundation

for vulnerability to suffering and pain proneness; these experiences are hypothesized to lie dormant only to be triggered and expressed when a genuine organic painful condition is present. Others have elaborated that this form of therapy is appropriate for those who demonstrate certain psychological characteristics such as marked dependency, passivity, masochism, denial, regression, repressed anger, overt hostility, or neuroticism (Lakoff, 1983). Central to psychodynamic therapy, however, is the importance of influences on behavior of which the patient may not be aware (Perlman, 1996). Therapy involves gaining understanding of the patients world, especially developmental history, on which a dynamic model of pain can be formulated (Lakoff, 1983). Pain appears by most therapists following this tradition to be understood as a real problem, not simply symbolic or metaphorical. The themes in the therapy can range from discussion of early childhood experiences, such as relationships with family or the experience of physical or sexual abuse, to discussion of the expression, or lack thereof, of emotion. In part, the therapist and patient work together to release affect and may explore pain as in part a metaphor for underlying conflicts (Perlman, 1996). Therapy can utilize the patienttherapist relationshipas a method of facilitating change; the therapist works to establish and sustain a relationship that enables patients to change . The therapist aims to help the patient accept his or her pain as important but not a defin-ing aspect of the self, and as regrettable but nevertheless manageable.Through therapy the person becomes an individual with persistent pain, who is able to remove pain from the center of existence and find purpose instead of anguish (Grzesiak et al., 1996). Biopsychosocial Model The biopsychosocial approach holds that the experience of pain is determined by the interaction among biological, psychological (which include cognition, affect, behavior), and social factors (which include the social and cultural contexts that influence a persons perception of and re-sponse to physical signs and symptoms). Compared to either of the traditional biomedical or psychodynamic positions, the biopsychosocial approach posits a much broader, multidimensional, and complex perspective on pain. This is true for both acute and chronic pain, although it is in the case of the latter that the model has proven most heuristic (Asmundson G.J.G. & Wright K.D., 2004,pp 42). The biopsychosocial model focuses on illness rather than disease. llness behavior is a term used to describe the ways in which given symptoms may be differently perceived, evaluated, or acted (or not acted) upon by different kinds of persons (Mechanic, 1962, p. 189; cf: Asmundson G.J.G. & Wright K.D., 2004,pp 42).Illness is seen as a result of a complex interaction of biological, psychological and social variables. The main tenet of this model is that there is a continuing, dynamic and reciprocal interplay between these variables, which shapes the patients perceptions and response to disease and pain. From this perspective, the diversity in illness expression is accounted for by the complex interrelationships among those variables (Caris, H.F.,2002). One of the hallmarks of the biopsychosocial perspective is the concept of evolution; at different points during the evolution of the pain experience, the weighting of the biological, psychological and social variables changes. Therefore, there is a distinction between the acute phase of pain experience and the chronic state experience of pain. During the acute phase, biological factors generally predominate, but over time psychological and social factors may gradually assume a disproportionate role in accounting for symptoms and disability. Therefore the role of the psychologist is less central, yet not insignificant, in the management of acute pain than it is in chronic or persistent pain management (Caris, H.F.,2002). One of the several of the most influential biopsychosocial approaches to chronic pain. These include the operant model, Glasgow model, biobehavioral model, and fear avoidance models. Operant Model Fordyce WE, Fowler RS, Lehmann JF & De Lateur BJ (1968) were the first to apply the behaviour model to pain (Innes , S.I.,2005). Behaviour theory defines pain by the presence of pain behaviours (Fordyce, 1976, 1986) which are

verbal and non-verbal signs of distress that are independent of subjective report. (Adams .N., Ravey .J.& Taylor.D.,1996.)Fordyce and colleagues (Fordyce, 1976; Fordyce, Shelton, & Dundore, 1982)detailed the operant conditioning model that describes how positive and negative reinforcement (i.e., presentation or removal of a stimulus, respectively) serve as mechanisms through which acute pain behaviors are maintained over time and thus become chronic(Asmundson G.J.G. & Wright K.D., 2004,pp.43)by positively reinforcing the pain behavior and not reinforcing the well behaviors. while well behaviour is not reinforced (Gamsa,1994 ,cf: Adams .N., Ravey .J.& Taylor.D.,1996). This model can be explained as follows: In response to an acute injury, people employ certain behaviors (e.g.,escape or withdrawal, avoidance of activity, limping) that serve an adaptive function in reducing likelihood of further tissue damage.These behaviors that reduce pain are negatively reinforced, in the short term, by the reduction of suffering associated with stimulation of nociceptors.Later, they can become persistent and maladaptive when the environment offers pain contingent reinforcement(Innes ,S.I.,2005) i.e., the reinforcement shifts from the reduction of nociceptive input to various external positive (e.g., increases social attention from family and friends) and negative (e.g., reduced degree of responsibility for completing tasks) reinforcers(Asmundson G.J.G. & Wright K.D., 2004,pp.43) thus providing secondary gains (Innes ,S.I.,2005). To add on,pain behaviour may also be learned by observing "pain models" i.e., individuals who exhibit such behavior (Innes ,S.I.,2005).Accordingly, chronic pain is viewed as a set of observable behaviors that persist beyond the time required for healing of physical pathology and lead to declines in physical activity and associated deconditioning, increases in use of analgesic medications, and the development of additional illness behaviors Although ,behaviour models have contributed to the study of pain by the introduction of carefully designed control procedures and laboratory methods ,more complex factors such as personal dynamics, emotional state, physical vulnerability, and numerous psychosocial variables were not addressed.Further , the question of what the patient is really experiencing is avoided in this model (Gamsa, 1994). Clinical applications Operant conditioning methods have become a fundamental part of successful pain rehabilitation, particularly in terms of increasing physical functioning (Caris, H. F., 2005). Sanders (1996) summarized the essential elements of the operant approach. The first component begins prior to the initiation of treatment and involves a functional behavioral analysis to identify relevant overt pain and well behaviors, and, as far as possible, antecedent stimuli and contingent consequences contributing to pain behavior. At this stage, patients are frequently encouraged to monitor and record their behavior (e.g., up and down time, walking, medication). Thereafter, operant treatment is described as involving several ingredients including: (a) response prevention for escape/avoidance behaviors; (b) positive and negative reinforcement (e.g., encouragement) to increase well behaviors from baseline (e.g., physical exercise, up time), with gradual reduction in this to a variable schedule once well behaviors are on the rise; (c) shaping or gradual change of well behaviors, which includes exercising to quota rather than exercising to tolerance; (d) elimination or reduction of factors that may maintain the overt pain behaviors outside the treatment environment, such as economic reinforcers, social attention, and avoidance of responsibilities; and (e) time-contingent delivery of medication while reducing the amount of medication per day (Hadjistavropoulos,H.D.,&Williams,A.C.C.,2004,pp.273). However, the mainstay of this approach is the targeting of behavioural excesses, as well as deficiencies, for intervention. Behavioural excesses are targeted for reduction or elimination, and for replacement by more adaptive behaviours. Behavioural deficits are targeted for remediation through shaping and positive reinforcement procedures. Operant conditioning methods are ideally used in concert with other psychological and medical treatments within an interdisciplinary team approach (Caris,H.F.,2005). In general, treatment components of operant behavior therapy include graded activation, time contingent medication schedules, and use of reinforcement principles to increase well behaviors and decrease maladaptive pain behaviors.

Psychologists can implement graded activity programs for chronic pain patients who have vastly reduced their activity levels (increasing likelihood of physical deconditioning) and subsequently experience high levels of pain upon engaging in activity. They are instructed to safely break the cycle of inactivity and deconditioning by engaging in activity in a controlled and time-limited fashion. In this manner, patients can gradually increase the length of time and intensity of activity to improve functioning. This approach is frequently embedded within cognitive-behavioral pain management treatments. Psychologists can institute time-contingent medication schedules to reduce the likelihood of dependence on pain medications for attaining adequate control over pain. Glasgow Model In an attempt to give equal emphasis to all components of the biopsychosocial approach, Waddell and colleagues (Waddell, 1987, 1991, 1992; Waddell, Main, Morris, Di Paoloa, & Gray, 1984; Waddell, Newton, Henderson,Somerville, & Main, 1993) applied the construct of illness behavior to chronic low back pain. They view chronic low back pain as a form of illness behavior stemming from physiological impairment (defined as pathologic, anatomic, or physiologic abnormality of structure or function leading to loss of normal body ability; Waddell, Somerville, Henderson, & Netwon, 1992) and influenced by cognition, affect, and social factors (cf: Asmundson G.J.G. & Wright K.D., 2004,pp.44). Biological and psychological factors interact (within the context of a larger social environment) in a manner that promotes chronic illness (or pain) behavior and, ultimately, disability. Social factors, although not explicit, impact on the interpretation of nociception as well as illness behaviors. The elements of the model can also be illustrated as a biopsychosocial cross section of a persons clinical presentation at a single point in time (Asmundson G.J.G. & Wright K.D., 2004,pp.45).Further, glasgow model recognizes that physical pathology (whether or not currently identifiable) plays an important precipitating role, and that the ongoing physiological impairment (e.g., muscular deconditioning) can give rise to nociception that is distinct from the original physical pathology.) Waddell (1991, 1992) reviewed the literature related to the Glasgow model. Empirical investigations examining the importance of active exercise in rehabilitation of low back pain have, for the most part, yielded results that provide confirmation of its validity. Waddell (1992) identified 13 out of 17 controlled studies that showed statistically and clinically significant benefits in pain, disability, physical impairment, cardiovascular fitness, psychological distress, or work loss as a result of the implementation of the active exercise approach (i.e., progressive increase in activity through exercise). Additionally, controlled trials comparing a combined behavioral/rehabilitation approach to physical exercise alone in the treatment of low back pain have also provided support for this model. Cognitive Theories Cognitive approaches were inspired in part by Melzack and Wall's (1975) gate control theory, which established a role for the cognitive-evaluative process in the modulation of pain. Cognitive theory examines constructs such as expectations and beliefs about pain, personal control, problem solving abilities and coping skills (Gamsa, 1994;cf : Adams .N., Ravey .J.& Taylor.D.,1996) and clearly states the relationship between cognition, affect and behavior. Since the mid 1970's proponents of cognitive theory studied the influence of the meaning of pain to patients, and examined the effect of coping styles on pain (Innes, S.I.,2005).The assumption of cognitive models of pain is that cognitive activity and an individuals emotional distress or behavioural difficulty is not a direct reaction to an untoward life event but rather a direct consequence of how that event is perceived.( Adams .N., Ravey .J. & Taylor.D.,1996) .Hence, it examines intervening variables such as attributions,expectations, beliefs, self-efficacy, personal control, attention to pain stimuli, problem solving, coping self-statements and imagery (Innes, S.I.,2005) Further, Ciccone and Grzesiak (1984) identified cognitive events which amplify pain syndromes to include catastrophising, over-generalisation, low frustration tolerance, external locus of control and mislabelling of somatic sensations .Though, the cognitive theory has added an important dimension to psychological research into pain, but the

influence of mental processes is only part of a complex problem (Gamsa, 1994) and proponents of this theory such as Turk et at! (1983) do not provide the solution (Adams ,N., Ravey, J. & Taylor ,D., 1996). Clinical Applications Cognitive therapy is a structured, time-limited, problem-focused, goal-oriented and educative form of psychotherapy; which is present (rather than past) oriented, stresses a collaborative relationship between therapist and patient, and encourages active participation in the treatment by both therapist and patient. It has been used in chronic pain management for 20 years and places specifically irrational ideas about pain and suffering at the forefront and suggests that the modification of these maladaptive beliefs is the central ingredient for a more successful adaptation to a life with chronic pain. The aim is to promote cognitive restructuring, facilitating a basic change in a persons perspective, attitudes, beliefs, emotional reactions and behaviours related to the pain they are experiencing. This entails teaching patients skills for identifying, evaluating and modifying the inner dialogue they maintain with themselves, in order to change the nature of the pain experienced favourably. This requires a sound motivation to change (Caris,H.M.,2002). For eg, the coping self-statement interventions educate patients regarding the negative impact of catastrophizing cognitions, and teach as an alternative the conscious engagement in positive coping self-statements during acute pain (e.g., I can handle this, The discomfort will go away quickly, Just relax) (Bruehl,S. & Chung,O.Y.,2004.pp.250). The sensory focus interventions encourage patients to focus exclusively on the sensations they are experiencing, thereby preventing activation of the emotional schema and resulting in a less intense pain experience (Logan, Baron, & Kohut, 1995;cf : Bruehl,S. & Chung,O.Y.,2004.pp.250). Distraction techniques consume part of an individuals limited capacity for atten-tion, thereby reducing the attentional resources that can be directed at the painful stimulus (McCaul & Malott, 1984). Review of the distraction litera-ture indicates that it is more likely to be effective for brief and lower inten-sity pain, and become less effective as the stimulus becomes longer lasting or more intense (McCaul & Malott, 1984) ( Bruehl, S. & Chung,O.Y.,2004.pp.250). Fear Avoidance Model Early fear-avoidance models (Lethem J, Slade PD, Troup JD, Bentley G,1983; Philips HC,1987; Waddell G, Newton M, Henderson I, et al.1993;cf : Turk,D.C.,& Wilson,H.D.,2011 ) conceptualized the role of pain and avoidance behavior as distinct from the sensory component of pain. Mainly, they proposed that avoidance of pain was not directly related to current pain severity, but rather was the result of specific expectancies, beliefs, and interpretations surrounding the perception of pain. These models stressed the reciprocal interaction between affective states and cognitive-interpretive processes -the idea that thinking affects mood and mood influences appraisals, thereby affecting the experience of pain (Turk,D.C.,& Wilson,H.D.,2011). Contemporary fear-avoidance models (Asmundson, G.; Norton, P.; Vlaeyen, J.,2004; Vlaeyen JW, Kole-Snijders AM, Boeren RG, van Eek H.,1995; McCracken LM, Zayfert C, Gross RT.,1992;cf : Turk,D.C.,& Wilson,H.D.,2011) have expanded on these earlier conceptualizations through expansion of the cognitive and affective constructs thought to be involved in pain perception and experience.This model states that pain perceptions (eg, a physical injury, migraine headache) interact with predispositional factors (eg, anxiety sensitivity, genetic risk factors) to result in individual pain expression. Pain expression is also influenced by environmental factors (eg, disability compensation system, social support). People may have low pain-related fear, such that they do not stop all activities and adopt the belief that activity will always result in pain or further injury. In this case, people will continue activities, have confirming experiences that pain does not always equal harm, and maintain their quality of life. Alternately, people may catastrophize about the causes surrounding their pain, and have high pain-related fear. This begins the negative feedback cycle of pain: fear-avoidance and cessation of activity, leading to disuse, disability, and depression.

Self discrepencies & Self Enmenshment Theories Due to pain-related fear, the emerging avoidance behaviour and disability may in fact increase the discrepancy between the major life goals of the individual and the actual situation. These kinds of discrepancies are known to affect a persons experience of self and identity. The self-discrepancy theory and self-pain enmeshment theory both elaborate on the effects of discrepancies (Karoline Lisette Helena Vangronsveld,2007). Some studies found evidence for the association between dejection-related emotions and agitation-related emotions and different types of discrepancies (Waters et al., 2004; Morley et al., 2005a). People will undertake actions or set goals to either approach an ideal or ought self or avoid a feared self. These approach and avoidance behaviours could be linked to or guided by specific fears, such as fear of movement and pain catastrophizing, both factors included in the fearavoidance model. Pain is likely to interfere with daily activities as well as major life goals. Self-discrepancies could be of influence on the transition from acute to chronic pain. They may also be of influence on the development of negative mood and avoidance behaviour and on persistence behaviour by means of a constant drive of relieving the discrepancy (Karoline Vangronsveld,2007) Further the self-pain-enmeshment model builds on the principle of the three Is: Interruption, Interference, and Identity (Morley and Eccleston, 2004). Pain demands attention and interrupts ongoing activities and then later interfere with daily functioning, which when becomes repeated quite often will lead to an impact on self-schemata and thereby on identity. Thus, when pain becomes chronic interfering repeatedly with major goals in life, it will have an impact on the selfschemata and, thereby on the persons identity. That is the cognitive self-representations will become more and more enmeshed with cognitive representations about pain. The identity of the person is being taken over by pain and important aspects of the self are trapped by pain (Pincus and Morley, 2001; Waters et al., 2004; Morley et al., 2005b;cf : Karoline Vangronsveld,2007). Clinical Application Treatments aimed at breaking the fear-avoidance cycle employ systematic graded exposure to feared activities to disconfirm the feared, often catastrophic, consequences of engaging in activities. Graded exposure is typically supplemented with psychoeducation about pain and cognitive restructuring elements that target maladaptive cognitions and expectations about activity and pain.( Roditi,D. & Robinson,M.,2011). Psychologists are in an excellent position to execute these types of interventions that closely mimic exposure treatments traditionally used in the treatment of some anxiety disorders.Further, although in-vivo exposure treatments are superior at reducing pain catastrophizing and perceptions of harmfulness of activities, exposure treatments seem to be as effective as graded activity interventions in improving func-tional disability and chief complaints(Leeuw M, Goossens ME, van Breukelen GJ, et al.2008; cf : Roditi,D. & Robinson,M.,2011). Biobehavioral Model The first model of pain to comprehensively incorporate both cognitive and behavioral elements was proposed by Turk, Meichenbaum, and Genest (1983). The initial model was an attempt to extend the behavioral conceptualization posed by Fordyce (1976), based on the influential writings on cognitive therapy published in the latter part of the 1970s (e.g., Beck, 1976; Meichenbaum, 1977). More recently, Turk and colleagues (Turk, 2002; Turk & Flor, 1999) described the model using the term biobehavioral, where bio refers to biological factors and behavioral to a broad spectrum of psychological and sociocultural factors. The biobehavioral model suggests that chronic pain problems are the product of an interaction between a necessary predisposition and specific (learned) cognitive, behavioral, social, and physiological response patterns to pain sensations and other stressors as well as subsequent maladaptive responses to resulting distress. In this context, then, it is the persons anticipation of and response to distress, not nociceptive input itself, that leads some to experience chronic pain and associated disability

The chronic pain problems due to the interaction includes conditioned and unconditioned autonomic nervous system (comprising sympathetic and para-sympathetic divisions), sensitization of central nervous system structures, and muscular responsivity, as well as avoidance behavior, when appraisals are negative and coping resources are insufficient. The type (i.e., the specific symptom manifestation) and persistence of the illness problem that develops are determined, in part, by the way in which one attends and responds to nociception. Further, a variety of learning processes, the meaning ascribed to symptoms (through processes such as expectancies, hypervigilance, preoccupation, misinterpretations of catastrophic nature, fear), avoidance behavior, social interaction (e.g., the way in which ones significant others respond to their pain), and subsequent alterations in physiological responsivity (e.g., persistent sympathetic nervous system activation; persistent muscular reactivity) play an important role in maintenance and exacerbation of symptoms. Cognitive Behavioral Theory The cognitive-behavioral model of chronic pain takes into account the complex interactions among the cognitive, behavioral, affective, social, and sensory -physical aspects of the pain experience (Novy D,2004 ;cf : Osborne,T.L., Raichle,K.A. & Jensen,M.P.,2006). This model acknowledges the important roles that learning and behavior (eg, environmental responses to pain behaviors ) play in patient functioning but also argues that cognitions (eg, attribut ions, beliefs) can enhance or interfere with effective behavioral coping (Osborne,T.L., Raichle,K.A. & Jensen,M.P.,2006). Thus,it draws upon such areas as behaviourism, social learning theory and cognitive psychology (Grzesiak and Perrine, 1987;cf : Adams .N., Ravey .J. & Taylor.D.,1996). Though, they do not offer a model of the causes of the pain, they do explain how chronic pain can be made worse or maintained by psychological factors. Both assessment and treatment are highly individualised, based on patients pain behaviours, conceptualisation of the pain problem, and ability to cope with the stresses related to pain. The cognitive behavioural model thus views the way in which individuals react to pain as a complex, multidimensional response. Thus, it emphasizes the role of the individual's beliefs about and meanings attributed to various aspects of the experience of pain. The model is fully interactive, borrowing the language of a transactional perspective, where all aspects of the experience are in a continuous reciprocal determinism and wherein the individual is continually appraising and interpreting his or her experience to define it (Bandura, 1977; Folkman & Lazarus, 1980; Lazarus & Folkman, 1984; Turk etal., 1983;cf : Novy,D.M., & Nelson, D.V., Francis, D.J., Turk, D. C., 1995). Because of the emphasis placed on cognitive factors, the cognitive-behavioral perspective sometimes reads as if cognition is the most salient constituent of the pain experience; however, there is generally an attempt to temper this impression by emphasizing the continuously interactive nature of the pain experience, thereby rendering it fruitless to attempt to identify any one constituent of the experience as more important than any other (Turk et al., 198 3; Turk & Rudy, 1986;cf : Novy.et.al.,1995). Clinical Applications Cognitive-behavioral therapy (CBT) interventions for chronic pain utilize psychological principles to effect adaptive changes in the patients behaviors, cognitions or evaluations, and emotions. The overarching goal is to increase the patients understanding of their pain and their efforts to manage pain and its sequelae in a safe and adaptive manner; therefore, teaching patients to self-monitor their behavior, thoughts, and emotions is an integral component of therapy and a useful strategy to enhance self-efficacy. An appealing feature of the cognitive behavioral approach is its endorse-ment of the patient as an active participant of his/her pain rehabilitation or management program (Roditi, D. & Robinson,M.,2011). These interventions are generally comprised of basic psychoeducation about pain and the patients particular pain syndrome, several behavioral components, coping skills training, problem-solving approaches, and a cognitive restructuring component, though the exact treatment components vary according to the clinician. Behavioral

components may include a variety of relaxation skills (as reviewed in the behavioral approaches section), activity pacing instructions/graded activation, behavioral activation strategies, and promotion of resumption of physical activity if there is a significant history of activity avoidance and subsequent deconditioning. The primary aim in coping skills training is to identify current maladaptive coping strategies (eg, catastrophizing, avoidance) that the patient is engaging in alongside their use of adaptive coping strategies (eg, use of positive self-statements, social support) . Throughout treatment, problem-solving techniques are honed to aid patients in their adherence efforts and to help them increase their self-efficacy. Cognitive restructuring entails recognition of current maladaptive cognitions the patient is engaging in, challenging of the identified negative cognitions, and reformulation of thoughts to generate balanced, adaptive alternative thoughts. Additional components sometimes included in a CBT intervention include social skills training, communication training, and broader approaches to stress management. Via a pain-oriented CBT intervention, many patients profit from improvements with regard to their emotional and functional well-being, and ulti-mately their global perceived health-related quality of life (Roditi,D. & Robinson,M.,2011). Further, Acceptance and commitment therapy (ACT) ,the most common of the acceptance-based psychotherapies identified as third-wave cognitive-behavioral therapies emphasizes the importance of facilitating the clients progress toward attaining a more valued and fulfilling life by increasing psychological flexibility rather than strictly focusing on restructuring cognitions (Blackledge, J.T. & Hayes, S.C.,2001;cf : Roditi,D. & Robinson,M.,2011). In the context of chronic pain, ACT targets ineffective control strategies and experiential avoidance by fostering techniques that establish psychological flexibility. The six core processes of ACT include: acceptance, cognitive defusion, being present, self as context, values, and committed action (Hayes, S.C., Luoma, J.B., Bond, F.W. ,Masuda, A. & Lillis, J.,2006;cf : Roditi,D. & Robinson,M.,2011) which are used in conjunction with one another to take a holistic approach toward increasing psychological flexibility and decreasing suffering.Therefore,patients are encouraged to view pain as inevitable and accept it in a nonjudgmental manner so that they can continue to derive meaning from life despite the presence of pain. The interrelated core processes exemplify mindfulness and acceptance processes and com-mitment and behavior change processes (Hayes, S.C., Luoma, J.B., Bond, F.W. ,Masuda, A. & Lillis, J.,2006;cf : Roditi,D. & Robinson,M.,2011). Psychophysiological Models These models consider the interaction of physiological and psychological factors in the development of chronic pain. Psychophysiological studies examine the influence of mental events (thoughts, memories and emotions) on physical changes which produce pain (Gamsa, 1994). The possible role of physical responses such as muscle activity, vascular changes or autonomic arousal has been studied extensively in relation to pain disorders such as headaches (Andrasik and Holroyd, 1981), myofascial pain and low back pain (Flor et al, 1991; Arena et all 1991), with inconsistent findings (Gamsa, 1994) (cf : Adams .N., Ravey .J. & Taylor .D., 1996). In explaining the mechanisms which link abnormal psychophysiological patterns with pain, two general models are proposed. First, general arousal models propose that frequent or prolonged arousal of the autonomic nervous system, including prolonged muscle contraction, generate and perpetuate pain. In contrast, specificity models explain the development of specific types or sites of pain in relation to inter-individual differences in psychophysiological responses to environmental stressors due to genetic predisposition, previous experiences and personality type (Schneider and Wilson, 1985;cf : Adams .N., Ravey .J. & Taylor .D., 1996). The mechanisms involved, however, are not well understood (Adams .N., Ravey .J. & Taylor .D., 1996 ). Clinical Applications Some of the techniques which are based on this theory include biofeedback, relaxation training, hypnosis, etc. The goal of biofeedback approaches is for the patient to learn how to initiate physiological self- regulatory processes by achieving voluntary control over certain physiological responses to ultimately increase physiological flexibility through greater awareness and specific training. Thus a patient will use specific self-regulatory skills in an attempt to reduce an undesired

event (eg, pain) or maladap-tive physiological reactions to an undesired event (eg, stress response). Studies have provided empirical support for biofeedback for TMD, albeit more robust improvements with regard to pain and painrelated disability have been found for protocols that combine biofeedback with cognitive behavioral skills training, under the assumption that a combined treatment approach more comprehensively addresses the gamut of biopsychosocial problems that may be encountered as a result of TMD (Gardea ,M.A., Gatchel, R.J.& Mishra ,D.,2001). The focus of relaxation training is to reduce tension levels (physical and mental) through activation of the parasympathetic nervous system and through attainment of greater awareness of physiological and psychological states, thereby achieving reductions in pain and increasing control over pain. Patients can be taught several relaxation techniques and practice them individually or in conjunction with one another, as well as adjuvant components to other behavioral and cognitive pain management techniques.The various relaxation techniques include Diaphragmatic breathing, Progressive muscle relaxation, Autogenic training and visualization/Guided imagery (Roditi,D. & Robinson,M.,2011). There is usually some overlap between relaxation and hypnosis and these techniques are commonly blended as needed. Various hypnotic techniques have also been applied to management of acute pain. These techniques incorporate aspects of both traditional relaxation procedures and imagery training, in combination with suggestions .In acute pain situations, where long-term coping with pain is unnecessary, hypnosis can be used to obtain relief by actively moving the patients mind to comfort and pleasure unrelated to symptoms (Bruehl,S. & Chung,O.Y.,2004.; Roditi,D. & Robinson,M.,2011). Integrated Diathesis-Stress Model The consistencies and themes apparent in all the biopsychosocial models (operant, Glasgow, biobehavioral, and contemporary fear-avoidance models) include recognition of the importance of some physiological pathology (which may not remain the same as that associated with initial nociception); some form of vulnerability (diathesis); a tendency to catastrophically misinterpret somatic sensations and respond to them in maladaptive ways; and the development of a selfreinforcing vicious cycle that serves to exacerbate and maintain symptoms and functional disability.These are integrated into the current model proposed by Asmundson G.J.G. & Wright K.D.( 2004) which recognizes the importance of physiological, psychological, and sociocultural factors in the etiology, exacerbation, and maintenance of chronic pain. Interactions between various factors are clearly indicated and, can lead to a vicious, self-reinforcing cycle that influences and is influenced by distress and functional disability. An initial physical pathology or injury is recognized as necessary to nociception and the appraisal that set the cycle in motion. Also necessary is a predispositional vulnerability factor (diathesis). The difference between those who become distressed and disabled and those who dont is presumed to lie in the manner in which nociception is appraised and responded to. Those with a predisposition that reduces threshold for nociceptive activation and increases the tendency to respond with fear to bodily sensations (i.e., anxiety sensitivity, illness sensitivity) are more likely to respond to pain sensations with anxious apprehension (i.e., a future-oriented preparedness to cope with upcoming negative events or experiences). In turn, they develop cognitive and behavioral repertoires that serve to maintain this preparedness. Also, physiological stimulation shifts from nociceptive input of the precipitating pathology or injury to that stemming from autonomic nervous system and muscular activation. Learning processes contribute not only to the maintenance of the vicious cycle, but to anxious anticipation regarding events only remotely associated with pain-specific distress and disability. Thus, a general sense of perceived readiness for and inability to influence personally relevant events and outcomes develops. Those without the necessary predisposition appraise their pain sensation as nonthreatening, do not respond with maladaptive cognitive or behavioral repertoires, and in most cases recover (Asmundson G.J.G. & Wright K.D., 2004).