discussion #9 disease

If we liken models of pain to facial displays of emotion, it becomes readily

apparent that many expressions have evolved. Indeed, over the years there

have been a large number of models proffered by individuals from varying

intellectual traditions. Most of these models can be grouped within one of

several general categories—traditional biomedical, psychodynamic, and

biopsychosocial. The intent of all models, without exception, has been to

address the enduring questions of “What is pain?” and “How do we best al-

leviate pain and the suffering associated with it?” The primary purpose of

this chapter is to gain insight into answers to these questions by exploring

various iterations of the biopsychosocial approach and related empirical

literature.

To date, there have been a number of reviews written on biopsycho-

social approaches to pain (e.g., Robinson & Riley, 1999; Turk, 1996a; Turk &

Flor, 1999; Waddell, 1991, 1992). Nonetheless, the face of pain, or at least the

way we as clinical and research psychologists view it, is constantly chang-

ing. Indeed, many of the earlier models have proven inadequate for patient

care, and more recent research has superseded initial formulations. Take,

for example, the advancement of the original conceptualizations of the gate

control theory (Melzack & Casey, 1968; Melzack & Wall, 1965, 1982)—the first

to integrate physiological and psychological mechanisms of pain—to the

current neuromatrix model as described by Melzack and Katz in chapter 1

of this volume. Similar progress has occurred in the context of biopsy-

chosocial approaches that have emerged from postulates of the gate con-

C H A P T E R

2

Biopsychosocial Approaches to Pain

Gordon J. G. Asmundson Faculty of Kinesiology and Health Studies

and Depar tment of Psychology, University of Regina

Kristi D. Wright Depar tment of Psychology, University of Regina

35

trol theory, such that our answers to the “what” and “how” questions just

posed are, in our opinion, becoming more clear. To this end, the concepts

presented herein provide an important piece of the foundation on which

the assessment and treatment approaches described in other chapters of

this volume are built.

Our intent in this chapter is to provide an overview and critical analysis

of the traditional biomedical and psychodynamic models, summarize ele-

ments of the gate control theory that strongly influenced current conceptu-

alizations of pain, and review important details of models that fall under the

biopsychosocial rubric. Within the context of the latter, we include discus-

sion of some of the most influential behavioral, cognitive, and cognitive-

behavioral models and associated empirical findings. We conclude by posit-

ing a synthesis of the various iterations of the biopsychosocial approach,

place this in the context of a comprehensive diathesis–stress model (i.e., a

model in which dispositional tendencies to respond to stressors in a certain

way interacts with stressors to produce illness behavior), and briefly dis-

cuss its implications for future research.

TRADITIONAL BIOMEDICAL MODEL

The traditional biomedical model of pain dates back hundreds of years.

Descartes (1596–1650) modernized it in the 17th century (Bonica, 1990; Turk,

1996a), and in that form it held considerable influence through to the mid

20th century. The model holds, in essence, that pain is a sensory experi-

ence that results from stimulation of specific noxious receptors, usually

from physical damage due to injury or disease (see Fig. 2.1). Consistent with

Cartesian dualism (i.e., the idea that mind and body are nonoverlapping en-

tities), the model has been described by some (e.g., Engel, 1977; Turk &

Flor, 1999) as being both reductionistic (i.e., assumes that all disease is di-

rectly linked to specific physical pathology) and exclusionary (i.e., assumes

that social, psychological, behavioral mechanisms of illness are not of pri-

mary importance).

Consider the case of Jamie, a middle-aged person with strained muscles

in the low back. Applying the traditional biomedical model, the method of

36 ASMUNDSON AND WRIGHT

FIG. 2.1. Schematic of traditional medical model.

diagnosing and subsequently treating Jamie should be, for all practical pur-

poses (and notwithstanding availability of adequate diagnostic, surgical,

and pharmacologic technology), straightforward. Jamie’s physical pathol-

ogy would be confirmed by data obtained from objective tests of physical

damage and, if thorough, tests of impairment. Medical interventions would

then be directed toward rectifying the muscle strain. The impact of the

strain on Jamie’s social, psychological, and behavioral functioning would

not be given much weight in any intervention. Indeed, other symptoms re-

ported by Jamie, such as depressed mood, hypervigilance to somatic sensa-

tions, and pain, would not be viewed as significant but, rather, as secondary

reactions to (or symptoms of ) the muscle strain. These would be expected

to subside after the muscle strain had healed.

In Jamie’s case, intervention was targeted at healing the muscle strain

and all symptoms subsided within 5 weeks. But, for every Jamie there is an-

other person for whom application of an identical intervention does not re-

solve pain and other symptoms, including disability, despite eventual heal-

ing of physical pathology. Why? As becomes evident in this chapter, the

reductionistic and exclusionary assumptions of the biomedical models

have not been upheld. We now know that pain involves more than sensa-

tion arising from physical pathology. Indeed, many people with persistent

pain, including perhaps the majority with low back pain, will never have

had an identifiable medical diagnosis of tissue damage.

Most 20th-century models of pain, including amendments to the tradi-

tional biomedical model (e.g., Bonica, 1954; Hardy, Wollf, & Goodell, 1952),

recognize to some degree that factors such as cognition and emotional

state are important in the experience of pain. These models were not with-

out criticism. For example, they posited a primary role for sensation and

did not recognize the possibility that sensation and affect might be proc-

essed in parallel (Craig, 1984). Still, they demarcated a beginning to the rec-

ognition of the interplay between biological, psychological, and sociocul-

tural factors in the pain experience. Before turning attention to integrated

multidimensional models of pain, we lay more of the groundwork by taking

a look at models of the psychodynamic tradition.

PSYCHODYNAMIC MODELS

The psychodynamic model can be considered to be among the first to posit

a central role for psychological factors in pain (see Merskey & Spear, 1967),

albeit with an emphasis on persistent (or chronic) rather than acute pres-

entations. A number of psychodynamic models have been proposed over

the years (e.g., Blumer & Heilbronn, 1981; Breuer & Freud, 1893–1895/1957;

Engel, 1959). These models are similar in that, unlike the traditional biomed-

2. BIOPSYCHOSOCIAL APPROACHES TO PAIN 37

ical model, they shift focus from physical pathology by conceptualizing per-

sistent pain as an expression of emotional conflict. Rather than review all of

the psychodynamic models, we provide an overview of the influential mod-

els of Freud (Breuer & Freud, 1893–1895/1957) and Engel (1959).

Freud (Breuer & Freud, 1893–1895/1957) held that persistent pain was

maintained by an emotional loss or conflict, most often at the unconscious

level. Central to Freud’s model was the process of conversion, or express-

ing emotional pain (i.e., the unresolved conflict) by converting it into physi-

cal symptoms that were a symbolic and more tolerable expression of the

underlying emotional issues. To illustrate, a women reporting dyspareunia

(i.e., persistent genital pain associated with sexual intercourse) may be

thought to be expressing some unresolved unconscious conflict regarding

taboo sexual urges, such as having sex with her sister’s husband. Freud be-

lieved 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.

In 1959 Engel introduced the concepts of psychogenic pain and the pain-

prone personality to further explain the nature of persistent pain. The key el-

ements of Engel’s position were that (a) persistent pain can, but need not,

have a basis in physical pathology, and (b) in some people, it is a psycho-

logical phenomenon that serves a self-protective function. It is pain in the

absence of identifiable physical pathology that has, since Engel’s (1959)

contribution, been referred to by many as psychogenic, or of psychological

origin. Most often the decision is made on the basis of exclusion; that is, in

the absence of identifiable pathology, it is presumed emotional conflict

must explain the symptoms.

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. For exam-

ple, early in life a person may learn to associate pain with others’ responses

to his or her behavior (e.g., affection in response to crying, punishment in

response to inappropriate behavior, aggression). Later in life, the person

may use pain as an unconscious defense against various bouts of emotional

distress he or she experiences (much as posited by Freud). Although the

former of these propositions was supported in part by findings from empiri-

cal tests of social learning influences on pain (e.g., Craig, 1978), the latter re-

mains controversial.

What type of person is most likely to do this or, in other words, to have a

pain-prone personality? Engel (1959) suggested that those with psychiatric

conditions, as described by diagnostic nomenclature of the day (e.g., DSM–I

provided for the possibilities of hysteria, major depression, hypochon-

driasis, or paranoid schizophrenia), were particularly prone to experience

38 ASMUNDSON AND WRIGHT

persistent pain. Amendments to Engel’s model, such as Blumer and Heil-

broon’s (1982) position on chronic pain as a variant of major depressive dis-

order, 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. The results of a large number of studies suggest that the

prevalence of current psychiatric conditions is, indeed, elevated in patients

with chronic pain relative to base rates in the general population (e.g.,

Asmundson, Jacobson, Allerdings, & Norton, 1996; Dersh, Gatchel, Polatin,

& Mayer, 2002; Katon, Egan, & Miller, 1985; Large, 1986). 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 Nerv-

ous and Mental Disease, and Large, 1986).

With few exceptions (Adler, Zlot, Hürny, Minder, 1989), the psychody-

namic formulations have not fared well against empirical scrutiny (see re-

views by Gamsa, 1994; Large, 1986; Roth, 2000; Roy, 1985), and now have di-

minished popularity in mainstream psychology. Notwithstanding, they did

play a key role in drawing attention to the importance of psychological (and

contextual) factors in the experience of pain at a time when treatment for

pain was primarily directed by the biomedical model. This attention led to

increased and continuing research into a wide array of psychosocial vari-

ables (e.g., birth order, childhood abuse, interpersonal and marital difficul-

ties, depression, anxiety, personality disorders, illness behavior), their role

in the development and maintenance of chronic pain, and their importance

in contemporary psychological treatment formulations. Indeed, the interest

in psychological factors spawned by psychodynamic theorists served as an

essential precursor to the development of contemporary biopsychosocial

approaches. However, using Roth’s (2000) analogy of the double-edged

sword, it is noteworthy that there are lingering and unwanted scars of this

psychodynamic thrust. These include the general tendency to assume (a)

that all cases of pain in the absence of identifiable physical pathology are

the result of psychological factors, and (b) that these are equally relevant

to all people with persistent pain. Although incorrect, these assumptions

can (and still often do) have a negative impact on opinions and general

treatment of people who suffer from persistent pain conditions.

GATE CONTROL THEORY

As noted earlier, Melzack and colleagues’ seminal papers on the gate con-

trol theory of pain (Melzack & Casey, 1968; Melzack & Wall, 1965) are fre-

quently cited as the first to integrate physiological and psychological mech-

2. BIOPSYCHOSOCIAL APPROACHES TO PAIN 39

anisms of pain within the context of a single model. It is beyond the scope

of this chapter to provide a detailed synopsis of the theory; however, given

its contribution to current conceptualizations of pain, a brief overview is

warranted.

Melzack and Wall (1965) proposed that a hypothetical gating mechanism

within the dorsal horn of the spinal cord is responsible for allowing or disal-

lowing the passage of ascending nociceptive information from the periph-

ery 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 as-

cending fibers from the periphery with that traveling on descending fi-

bers from the brain determines whether the gate is open or closed and,

as such, influences the perception of pain.

Since this original proposal we have, of course, moved beyond believing

that the key to understanding pain is knowing what happens in the dorsal

horn. 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 recog-

nized 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 cog-

nitive information based on analysis of multimodal information, past experi-

ence, and probability of outcome of different response strategies” (pp.

427–428).

Think back to the case of Jamie, who had pain associated with muscle

strain in the low back. Applying the postulates of the gate control theory,

Jamie’s pain experience might be understood as follows: Stimulation of

nociceptors in the region of muscle strain facilitated transmission of infor-

mation along ascending fibers, through an open gate, and on to Jamie’s

brain. At the same time, Jamie’s brain was sending information about her

current cognitions and emotional state (i.e., depressed and hypervigilant)

back to the gate along descending fibers. The summation of the ascending

nociceptive input and descending information regarding cognition and

40 ASMUNDSON AND WRIGHT

emotion, in this case, kept the gate open. This process was ongoing (i.e., it

lasted for many days) and involved an interaction between physiological,

cognitive, and affective inputs that continuously modified Jamie’s percep-

tion of the pain. Medical and behavioral interventions ultimately served to

close the gate, reducing pain, and improving Jamie’s mood state and overall

functional ability.

Based on this brief overview it should be apparent that the gate control

theory challenged the primary assumptions of the traditional biomedical

and psychodynamic models. Rather than being exclusively conceptual-

ized as sensation arising from physical pathology or somatic manifesta-

tion of unresolved emotional conflicts, the experience of pain came to be

viewed as a combination of both pathophysiology and psychological fac-

tors. On this basis, then, Jamie’s depressed mood would not be viewed as

a secondary reaction to pain, nor would the pain be viewed as a result of

depressed mood. Rather, each would be seen as having a reciprocal influ-

ence on the other.

The assumptions of the gate control theory have not gone unchallenged,

and advances in our understanding of the anatomy and structure of the

gating mechanism have led to various revisions. The details of the changing

views of the physiology of the gating mechanism are beyond the intent and

scope of this chapter. We recommend that interested readers refer to arti-

cles in Supplement 6 of the 1999 volume of Pain entitled “A Tribute to Pat-

rick D. Wall” and to recent reviews written by Turk and Flor (1999) and Wall

(1996). Notwithstanding, the essential elements of the model, as described

earlier, have proven a heuristic of considerable value to both basic scien-

tists and clinical scientist-practitioners.

Melzack’s (1999) own words most accurately describe the most impor-

tant contribution of the theory:

Never again, after 1965, could anyone try to explain pain exclusively in terms

of peripheral factors. The theory forced the medical and biological sciences

to accept the brain as an active system that filters, selects and modulates in-

puts . . . we highlighted the central nervous system as an essential component

in the process. (p. S123)

Since 1965, but particularly over the past 25 years, there have been many

advances to our understanding of the specific nature of the psychological

and sociocultural factors of pain. For example, Price (2000) proposed a par-

allel-serial model of pain affect that is consistent with existing literature.

This model details a central network of brain structures (e.g., anterior

cingulate cortex, hypothalamus, insular cortex) and pathways (e.g., spino-

hypothalamic pathway, cortico-limbic somatosensory pathway), compris-

ing both serial and parallel connections, as the mechanism through which

2. BIOPSYCHOSOCIAL APPROACHES TO PAIN 41

the emotional valance of pain is determined and subsequently expressed.

Other important advances are succinctly captured in the context of Mel-

zack’s neuromatrix theory (see chap. 1, this volume), as well as in other

general models that focus on the cognitive, affective, and behavioral as-

pects of the pain experience.

THE BIOPSYCHOSOCIAL APPROACH

Turk and Flor (1999) have accurately and succinctly captured the basic

premises of the biopsychosocial approach to pain. They stated:

Predispositional factors and current biological factors may initiate, maintain,

and modulate physical perturbations; predispositional and current psycho-

logical factors influence the appraisal and perception of internal physiological

signs; and social factors shape the behavioral responses of patients to the

perceptions of their physical perturbations. (p. 20)

In short, 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 person’s perception of and re-

sponse to physical signs and symptoms). Compared to either of the tradi-

tional biomedical or psychodynamic positions, the biopsychosocial ap-

proach 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.

A number of specific iterations of the general biopsychosocial approach

to pain have been put forth over the years. Like similar models proposed to

account for other chronic health conditions (e.g., asthma, functional dys-

pepsia; tinnitus, Meniere’s disease; Asmundson, Wright, & Hadjistavrop-

oulos, 2000), these iterations are based on several assumptions, as follows:

� Unlike the traditional biomedical model, the focus is not on disease per

se but rather on illness, where illness is viewed as a type of behavior

(Parsons, 1951). Illness 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). This definition implies that there are individual differences

in responses to somatic sensations, and that these can be understood in

the context of psychological and social processes (Mechanic, 1962).

� Illness behavior is considered a dynamic processes, with the role of bio-

logical, psychological, and social factors changing in relative impor-

42 ASMUNDSON AND WRIGHT

tance as the condition evolves (also see Engel, 1977; Lipowski, 1983). Al-

though a condition may be initiated by biological factors, the psycholog-

ical and social factors may come to play a primary role in maintenance

and exacerbation. Also, as suggested earlier, there are individual differ-

ences in the relative importance of any given factor at any given time

during the course of a condition.

With these assumptions in mind, we now turn to several of the most influen-

tial biopsychosocial approaches to chronic pain. These include the operant

model, Glasgow model, biobehavioral model, and fear avoidance models.

We organize our presentation of these models in an ascending chronologi-

cal order. Empirical evidence is grouped according to degree of relevance

to the model under consideration; however, it should be noted that the

findings of some investigations have implications for more than one model.

THE OPERANT MODEL

Model Summary

Fordyce and colleagues (Fordyce, 1976; Fordyce, Shelton, & Dundore, 1982)

detailed an operant conditioning model that describes how positive and

negative reinforcement (i.e., presentation or removal of a stimulus, respec-

tively) serve as mechanisms through which acute pain behaviors are main-

tained over time and thus become chronic. The premises of this model are

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.

� Behaviors that reduce pain are negatively reinforced, in the short term,

by the reduction of suffering associated with stimulation of nociceptors.

� These behaviors can become persistent and maladaptive when rein-

forcement shifts from the reduction of nociceptive input to various ex-

ternal positive (e.g., increases social attention from family and friends)

and negative (e.g., reduced degree of responsibility for completing

tasks) reinforcers.

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 be-

haviors.

2. BIOPSYCHOSOCIAL APPROACHES TO PAIN 43

Empirical Overview

Evidence in support of the operant model has come primarily from studies

supporting operant-based treatment approaches (Block, Kremer, & Gaylor,

1980; Cairns & Pasino, 1977; also see recent meta-analysis by Morley, Eccles-

ton, & Williams, 1999), although this evidence is viewed by some as equivo-

cal (Sharp, 2001; Turk, 1996b). Despite this treatment-based evidence, there

have been few empirical tests of the validity of the operant model. Linton

and Götestam (1985), for example, conducted an experiment with adult hos-

pital employees exposed to a constant-level noxious stimulus while either

increases or decreases in verbal reports of pain from ischemic stimuli were

reinforced. Significant differences between reinforced increases and de-

creases in pain reports within subjects were observed. More recently, Flor

and colleagues (Flor, Knost, & Birbaumer, 2002) reinforced increases and

decreases in verbal pain reports in chronic back pain patients and matched

healthy controls exposed to electrical stimulation. Numerous physiological

indices were also evaluated. Results indicated that, despite similar learning

rates, the patients were influenced more by operant conditioning factors

than were the control subjects. Specifically, they were more likely to main-

tain elevated pain ratings and cortical responsivity (N150) during extinc-

tion. Others, however, have failed to show clear-cut operant conditioning ef-

fects (Lousberg, Groenman, Schmidt, & Gielen, 1996).

THE GLASGOW MODEL

Model Summary

In an attempt to give equal emphasis to all components of the biopsycho-

social approach, Waddell and colleagues (Waddell, 1987, 1991, 1992; Wad-

dell, 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. In Fig. 2.2 we

depict the essential features of the model as they relate to the case of Kelly,

who, like Jamie described earlier, had chronic back pain as well as de-

pressed mood and hypervigilance to somatic sensations subsequent to a

muscle strain. Unlike Jamie, Kelly’s pain persisted over several years.

The illustration shows how biological and psychological factors interact

(within the context of a larger social environment) in a manner that pro-

44 ASMUNDSON AND WRIGHT

motes 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 person’s clinical presentation at a

single point in time (see Fig. 2.3). Although not evident in either Fig. 2.2 or

2.3, it is noteworthy that the Glasgow model recognizes that physical pa-

thology (whether or not currently identifiable) plays an important precipi-

tating role, and that the ongoing physiological impairment (e.g., muscular

deconditioning) can give rise to nociception that is distinct from the origi-

nal physical pathology.

Empirical Overview

Waddell (1991, 1992) reviewed the literature related to the Glasgow model.

Empirical investigations examining the importance of active exercise in re-

habilitation 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 bene-

fits in pain, disability, physical impairment, cardiovascular fitness, psycho-

logical 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/rehabilita-

tion approach to physical exercise alone in the treatment of low back pain

have also provided support for this model.

2. BIOPSYCHOSOCIAL APPROACHES TO PAIN 45

FIG. 2.2. Application of the Glasgow model of chronic low back pain to illus-

trate Kelly’s clinical presentation.

Through theoretical analysis and literature review, coupled with results

from pilot studies, Waddell and colleagues (1993) concluded that the con-

cept of fear avoidance is a significant and driving factor within the context

of the biopsychosocial model of low back pain and disability. As such, the

core features of the Glasgow model were recently subsumed as a part of

the fear-avoidance models. The fear-avoidance literature is reviewed in

more detail later.

THE BIOBEHAVIORAL MODEL

Model Summary

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 conceptu-

alization posed by Fordyce (1976), based on the influential writings on cog-

nitive 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

46 ASMUNDSON AND WRIGHT

FIG. 2.3. Cross-sectional representation of the Glasgow model. Reprinted from

Waddell et al. (1993), “A Fear-Avoidance Beliefs Questionnaire (FABQ) and the

role of fear-avoidance beliefs in chronic low back pain and disability,” p. 164.

Copyright 1993. Reproduced with kind permission from Elsevier Science.

refers to biological factors and behavioral to a broad spectrum of psycho-

logical and sociocultural factors. The key elements of the model are sum-

marized as follows:

� Some people have a diathesis, or predisposition, for a reduced thresh-

old for nociceptive activation and a tendency to respond with fear to

bodily sensations. This diathesis may result from genetic makeup, so-

cial learning, prior trauma, or some combination of each.

� Aversive stimulation, whether related to nociception or some other

stressor (e.g., marital conflict, too many time demands), interacts with

the diathesis.

� The diathesis–stress interaction leads to conditioned and uncondi-

tioned autonomic nervous system (comprising sympathetic and para-

sympathetic divisions), sensitization of central nervous system struc-

tures, 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.

� A variety of learning processes, the meaning ascribed to symptoms

(through processes such as expectancies, hypervigilance, preoccupa-

tion, misinterpretations of catastrophic nature, fear), avoidance behav-

ior, social interaction (e.g., the way in which one’s significant others re-

spond 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.

To summarize, the biobehavioral model suggests that chronic pain prob-

lems are the product of an interaction between a necessary predisposition

and specific (learned) cognitive, behavioral, social, and physiological re-

sponse patterns to pain sensations and other stressors as well as subse-

quent maladaptive responses to resulting distress. In this context, then, it is

the person’s anticipation of and response to distress, not nociceptive input

itself, that leads some to experience chronic pain and associated disability.

Empirical Overview

Empirical studies of postulates of the biobehavioral model were recently re-

viewed by Turk and Flor (1999) and Turk (2002). Research in a number of ar-

eas substantiates the applicability of the biobehavioral model to the gene-

sis, maintenance, and exacerbation of pain. With respect to the notion of

2. BIOPSYCHOSOCIAL APPROACHES TO PAIN 47

diathesis, or predisposition, the presence of anxiety sensitivity (i.e., a dispo-

sition to respond with fear to somatic sensations) was suggested as a pre-

disposing factor in chronic pain (Asmundson, 1999; Asmundson, Norton, &

Norton, 1999; Muris, Vlaeyen, & Meesters, 2001). A positive association was

identified between anxiety sensitivity and pain-specific anxiety, avoidance

behaviors, fear of negative consequences of pain, and negative affect (Turk,

2000; also see Asmundson, 1999; Asmundson et al., 1999). In terms of the im-

pact of learning on behavior and pain perception, memories of somato-

sensory pain specific to a particular pain site have been found to form as a

result of chronic pain (Flor, Braun, Elbert, & Birbaumer, 1997). This forma-

tion was shown to manifest itself in an exaggerated portrayal of the affected

pain site in the primary somatosensory cortex. Further, learned memory

for pain was demonstrated in patients with phantom limb pain, such that

the amount of reorganization in cortical structures was shown to be pro-

portional to the magnitude of phantom leg pain (Flor et al., 1995).

Turk and Flor (1999) suggested that pain management programs that aim

to facilitate a patient’s ability to attribute success to his or her own volition

will result in long-term behavioral changes, and these, in turn, will impact

affective, cognitive, and sensory aspects of pain experience. Investigations

showed that these types of treatment programs do promote changes in

pain-specific beliefs, coping style, and behavior, as well as pain severity

(e.g., Arnstein, Caudill, Mandle, Norris, & Beasly, 1999; Buckelew et al., 1996;

Dolce, Crocker, Moletteire, & Doleys, 1986). Indeed, it was specifically dem-

onstrated that increased perceived control over pain and decreased catas-

trophizing are associated with decreases in pain severity ratings, functional

disability, and physiological activity (e.g., Jensen & Bodin, 1998; Jensen,

Turner, & Romano, 1991; Jensen, Turner, Romano, & Karoly, 1991; Sullivan

et al., 2001).

FEAR-AVOIDANCE MODELS

Model Summary

The role of fear and avoidance behavior as they relate to chronic pain have

received considerable attention over the past decade (for recent reviews,

see Asmundson et al., 1999; Vlaeyen & Linton, 2000). Indeed, the literature in

this area has grown to the point where state-of-the-art theory and research

are being published in the form of an edited book (Asmundson, Vlaeyen, &

Crombez, 2003). The postulates of fear-avoidance models have their roots

in early observations of significant anxiety in the pathology of pain (e.g.,

Paulett, 1947; Rowbotham, 1946), as well as in operant conditioning theory

(Linton, Melin, & Götestam, 1984; Fordyce, 1976) and its illness behavior

reformulations (Turk & Flor, 1999; Waddell et al., 1993).

48 ASMUNDSON AND WRIGHT

Several fear-avoidance models have been proposed to account for

chronic pain behavior. The fear-avoidance model of exaggerated pain per-

ception (Lethem, Slade, Troup, & Bentley, 1983), for example, attempted to

explain the process by which the emotional and sensory components of

pain become desynchronous (i.e., why fear and avoidance remain while tis-

sue damage remits) in some patients with chronic pain. Extending postu-

lates of the operant model of chronic pain, Philips (1987) incorporated ele-

ments of the cognitive theory of avoidance (Seligman & Johnson, 1973) to

explain cases where behavioral withdrawal was observed to continue in the

absence of adequate reinforcement. Avoidance was viewed as a product of

pain severity, a preference for minimizing discomfort, and cognitions (com-

prising expectancies, feelings of self-efficacy, and memories of past expo-

sures) that reexposure to certain experiences or activities will result in pain

and suffering.

Influenced by the work of Waddell et al. (1993), Letham et al. (1983), and

Philips (1987), and building on their earlier work (Linton et al., 1984;

Vlaeyen, Kole-Snijders, Boeren, & van Eek, 1995), Vlaeyen and Linton (2000)

proposed a comprehensive fear-avoidance model of chronic musculoskele-

tal pain. This model, illustrated in Fig. 2.4, can be summarized as follows:

2. BIOPSYCHOSOCIAL APPROACHES TO PAIN 49

FIG. 2.4. Fear-avoidance model. Reprinted from Vlaeyen and Linton, “Fear-

avoidance and its consequences in chronic musculoskeletal pain: A state of

the art,” p. 329. Copyright 2000. Reproduced with kind permission from the In-

ternational Association for the Study of Pain, 909 NE 43rd Ave, Suite 306, Seat-

tle, WA, USA.

� Injury initiates the experience of pain.

� If the experience is appraised as nonthreatening (e.g., viewed as a tempo-

rary hindrance that can be overcome), it is confronted and dealt with in

an adaptive manner that allows the person to proceed toward recovery.

� If the experience is appraised as threatening (e.g., a catastrophic event

that will never resolve), it may be dealt with in a maladaptive manner

that perpetuates a vicious fear–avoidance cycle that, in turn, promotes

disability.

In this context, then, confrontation is conceptualized as an adaptive re-

sponse that is associated with behaviors that promote recovery. Avoid-

ance, on the other hand, is viewed as a maladaptive response that leads to

a number of undesirable consequences. These include limitations in activ-

ity, physical and psychological consequences that contribute to disability,

continued nociceptive input (which, like the Glasgow model, may not neces-

sarily be related to original injury; also see Norton & Asmundson, 2003),

and further catastrophizing and fear.

Empirical Overview

Vlaeyen and Linton (2000) published a state-of-the-art review showing an

ever-increasing number of findings that corroborate postulates of fear-

avoidance models. Precursors of pain-related fear, including anxiety sensi-

tivity and health anxiety (i.e., the belief that bodily signs and symptoms are

indicative of serious illness), have been clearly identified. For example, in a

sample of chronic musculoskeletal pain patients, Asmundson and Taylor

(1996) found that anxiety sensitivity directly influences fear of pain, which,

in turn, directly influences self-reported escape/avoidance behavior. These

findings were replicated in adolescents (Muris et al., 2001) and adults with

heterogeneous pain complaints (Zvolensky, Goodie, McNeil, Sperry, & Sor-

rell, 2001). There is converging evidence demonstrating that fear of pain

affects the way people attend and respond to information about pain (As-

mundson, Kuperos, & Norton, 1997; Eccleston & Crombez, 1999; Hadjistav-

ropoulos, Craig, & Hadjistavropoulos, 1998; McCracken, 1997; Peters, Vlae-

yen, & Kunnen, 2002; Snider, Asmundson, & Weise, 2000). Likewise, there is

mounting evidence that fear of pain influences physical performance and is

more strongly related to functional disability than are indices of pain sever-

ity (Crombez, Vervaet, Lysens, Baeyens, & Eelen, 1998; Crombez, Vlaeyen,

Heuts, & Lysens, 1999; McCracken, Zayfert, & Gross, 1992; Vlaeyen et al.,

1995; Waddell et al., 1993). Finally, at the practical level, specifically treating

the “fear” component using techniques known to be effective in reducing

fears (i.e., graded exposure) has been shown to be most effective in reduc-

ing avoidance behavior and associated disability in patients with chronic

50 ASMUNDSON AND WRIGHT

musculoskeletal pain (Linton, Overmeer, Janson, Vlaeyen, & de Jong, 2002;

Vlaeyen, de Jong, Geilen, Heuts, & van Breukelen, 2001; Vlaeyen, de Jong,

Onghena, Kerckhoffs-Hanssen, & Kole-Snidjers, 2002).

TOWARD AN INTEGRATED DIATHESIS–STRESS MODEL

Our presentation of the various faces of pain shows, to a large degree, a de-

velopmental progression from the simplistic notions of somatogenic and

psychogenic causation through to the increasingly elaborate yet parsimoni-

ous postulates of the contemporary multidimensional, biopsychosocial ap-

proaches. In scanning the essential elements of the various models consid-

ered under the rubric of “biopsychosocial,” certain consistencies and

themes are apparent. These include recognition of the importance of (a)

some physiological pathology (which may not remain the same as that as-

sociated with initial nociception), (b) some form of vulnerability (diathesis),

(c) a tendency to catastrophically misinterpret somatic sensations and re-

spond to them in maladaptive ways, and (d) the development of a self-

reinforcing vicious cycle that serves to exacerbate and maintain symptoms

and functional disability. Taking an approach similar to that employed by

Sharp (2001) in his recent reformulation of Turk and colleagues biobe-

havioral model of pain (Turk, 2002; Turk & Flor, 1999; Turk et al., 1983), we

propose a model that integrates empirically supported elements of the op-

erant, Glasgow, biobehavioral, and contemporary fear-avoidance models.

This integrated stress–diathesis model is illustrated in Fig. 2.5.

It is important to keep in mind that pain and pain behaviors do not occur

in isolation. Rather, they are communicated in (see Hadjistavropoulos &

Craig, 2002) and influenced, for better or worse, by one’s social, interper-

sonal, and cultural milieu (e.g., Bates, Edwards, & Anderson, 1993; Craig,

1978). For example, a supportive environment can facilitate efforts to cope

with pain; however, if there is not enough or, indeed, too much support (i.e.,

where the “supporter” is overly solicitous), the overall pain experience is

likely to be aggravated. This appears to hold true for interactions with signifi-

cant others as well as those responsible for medical care, litigation, and

other such responses (see Sharp, 2001). Similarly, social modeling and social

learning experiences influence strongly the way in which one interprets and

responds to signs and symptoms of illness (e.g., Chambers, Craig, & Bennet,

2002; Craig & Prkachin, 1978; Martin, Lemos, & Leventhal, 2001). So, interpre-

tation and behavioral responses to pain depend, to some degree, on what is

learned from seeing others in pain and from cultural norms. This is recog-

nized, to varying degrees, in all of the biopsychosocial models discussed ear-

lier and provides the umbrella under which our model is placed.

2. METHODOLOGY IN WASHBACK STUDIES 51

As illustrated, our integrated diathesis–stress model recognizes the im-

portance of physiological, psychological, and sociocultural factors in the

etiology, exacerbation, and maintenance of chronic pain. Interactions be-

tween various factors are clearly indicated and, importantly, 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 recog-

nized 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 (like

Kelly) and those who don’t (like Jamie) is presumed to lie in the manner in

which nociception is appraised and responded to. Those with a predisposi-

tion 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 anx-

ious apprehension (i.e., a future-oriented preparedness to cope with upcom-

ing negative events or experiences). In turn, they develop cognitive and

behavioral repertoires that serve to maintain this preparedness. Also, phys-

iological stimulation shifts from nociceptive input of the precipitating pa-

thology or injury to that stemming from autonomic nervous system and

muscular activation. Learning processes contribute not only to the mainte-

nance of the vicious cycle, but to anxious anticipation regarding events

only remotely associated with pain-specific distress and disability. Thus, a

52 ASMUNDSON AND WRIGHT

FIG. 2.5. An integrated stress–diathesis model of chronic pain.

general sense of perceived readiness for and inability to influence person-

ally relevant events and outcomes develops. Those without the necessary

predisposition appraise their pain sensation as nonthreatening, do not re-

spond with maladaptive cognitive or behavioral repertoires, and in most

cases recover.

CONCLUSIONS

The primary intent of this chapter was to provide an overview of the vari-

ous expressions of pain that have been prominent over the years in ad-

dressing the enduring questions of “What is pain?” and “How can we allevi-

ate it?” Early models, whether physiological or psychological in focus, were

based on a unidimensional conceptualization. Subsequent to the seminal

contributions of Melzack and colleagues (Melzack & Casey, 1968; Melzack &

Wall, 1965), models moved toward a multidimensional conceptualization,

recognizing a complex interplay between physiological, psychological, and

sociocultural mechanisms in the pain experience. Today there are a num-

ber of heuristic biopsychosocial models, each holding (sometimes overlap-

ping) implications for understanding, assessing, and treating pain that per-

sists in the absence of identifiable physical pathology.

We have presented an integrated diathesis–stress model of chronic pain

founded, in part, on empirical support garnered from tests of other models,

in an attempt to emphasize the importance of interplay between biology,

cognition, affect, and social factors, as well as the key role of learning and

associated self-reinforcing feedback loops. In this context it should be clear

that simplistic notions of somatogenesis and psychogenesis are obsolete.

Our model, like its predecessors, yields a number of questions that, should

they be answered systematically, will serve to guide further advances in

both pain assessment and intervention strategies. What is the precise na-

ture of the diathesis? Is it genetic or learned? Can it be modified? To what

extend does anxious apprehension for pain-specific events and experiences

generalize to other sectors of a person’s life? Can we apply the models in a

way that allows identification of vulnerable or at-risk people prior to devel-

opment of chronic pain and associated disability? In other words, is preven-

tion feasible? In what ways do physiological reactivity serve to perpetuate

the cycle? What is the best method of intervention for those who become

mired in the vicious cycle? Graded in vivo exposure appears to have great

potential, but is there more to learn from the effective interventions of fun-

damental fears? How do we best address the influence of social influences

in the context of intervention? These are but a few of the questions that

await further investigation.

2. BIOPSYCHOSOCIAL APPROACHES TO PAIN 53

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