Efficacy and effectiveness of cognitive behaviour therapy for

chronic pain: progress and some challenges

Stephen Morley

University of Leeds, UK

Correspondence

Stephen Morley PhD, Leeds Institute of Health Sciences, University of Leeds, 101

Clarendon Road, Leeds LS2 9LJ, UK.

t: +44 113 343 2733;

e: s.j.morley@leeds.ac.uk

Published as:

Morley, S. (2011). Efficacy and effectiveness of cognitive behaviour therapy for

chronic pain: Progress and some challenges. Pain, 152(3, Supplement 1), S99-
S106. doi: 10.1016/j.pain.2010.10.042

1
Abstract

CBT is a class of treatments that have developed since the 1960s in response to

changing conceptualisations of the psychology of chronic pain and changing

conceptualisations of psychological change processes. Psychological processes

associated with the experience of pain range from the momentary processes

associated with attention and interruption to ongoing behaviour, interference in the

performance of essential social role, to the construction of self-identity. This article

briefly reviews the main features of contemporary CBT, summarises evidence for its

effectiveness and outlines the development of benchmarking for effectiveness

studies. Finally, attention is given to two areas that require further attention: (1) The

development of measures with clinically and socially significant referents of

outcome, and (2) procedures for assuring the quality of treatment implementation.

2
A very brief introduction to CBT

Cognitive behaviour therapy (CBT) is the dominant force in contemporary

psychological treatments for a very wide range of problems including chronic pain.

But what is CBT? Where did it come from? Can we regard it as a unified treatment?

How effective and efficacious is it in the field of chronic pain? What challenges face

practitioners and researchers in the field? The aims of this article are: to provide a

historically based brief review of the status of contemporary CBT for chronic pain; to

note the evidence for its efficacy from randomised controlled trials; to outline the use

of data from RCTs to provide benchmarks for routine clinical treatment and the

production of practice-based evidence; and to consider two substantial

methodological challenges – measurement of outcomes and the quality assurance of

treatment where progress in developing evidence can be made in routine clinical

practice.

In a recent review Gatchel and colleagues [20] provided a definition of CBT:

“The term CBT varies widely and may include self instructions … relaxation or biofeedback,

developing coping strategies, changing maladaptive beliefs about pain and goal setting …

varying selection of these strategies … embedded in a more comprehensive pain management

program that includes functional restoration, pharmacotherapy, and general medical

management.” Gatchel and colleagues are not alone in noting the broad remit of CBT

and its relative lack of specificity e.g. [12,73]. This definition does capture the

breadth of CBT, the mixture of techniques, aims and the variation in the context in

3
which CBT is practiced. To understand some of the key elements it is useful to see

how the main strands have developed and where they have been incorporated into

the field of pain.

TABLE 1 HERE

Table 1 uses a timeline to schematise major strands in contemporary CBT for

chronic pain beginning with the application of behaviour analysis by Fordyce in the

1960s [19] and ending with the introduction of Acceptance and Commitment

Therapy in the late 1990’s and from 2000 onwards [37]. The Table also indicates the

origins of each of the strands. Both Fordyce’s application of operant principles and

ACT have their roots in the analysis of respondent behaviour originating with

Skinner’s in the 1930s. Behaviour analysis established that much behaviour is a

function of two significant classes of external factors. The first class, reinforcement,

refers to consequences that determine the future probability of a specific behaviour.

The second class, antecedents, refers to the context in which behaviour occurs and

includes the presence of discriminative stimuli which signal the availability of

reinforcement. Fordyce’s insight was to recognise that although pain is essentially a

private experience there are publicly observable expressions of pain that are subject

to the influences of reinforcement and the context. As a consequence pain behaviour

may be modified in unhelpful ways. Similarly, it could be changed using the same

principles of reinforcement modifying the context. ACT is also grounded in the

experimental analysis of behaviour in particular the radical behavioural analysis of

4
the function of language and rule governed behaviour [22]. The complexity of ACT

is harder to grasp than the Fordyce’s earlier implementation but in essence the aims

are essentially the same, to change the control over behaviour that pain exerts by

altering the context.

By the beginning of the 1970s biofeedback and relaxation were introduced

into treatment protocols. Biofeedback also had its roots in the analysis of learning.

The experimental studies were concerned with a particular distinction between

classical (Pavlovian) conditioning and respondent (Operant) conditioning which

hypothesised that autonomic responses could not be operantly conditioned.

Paradoxically the first applications of biofeedback to pain disorder appear to have

been for chronic headache which targeted striated muscle [25]. Both biofeedback and

relaxation were incorporated into treatments for pain aimed at modifying the

hypothesised pain-tension-pain cycle. The recognition that complaints by many

patients might be construed as a stress response was also developed in the 1970s.

Elements of this analysis were drawn from the work in the preceding decade that

sought to elucidate factors responsible for the variation in responses to aversive

stimulation (stressors) by Lazarus and colleagues. This work established two crucial

ideas in the pain field, appraisal and coping, that are still current e.g. catastrophizing

and coping skills training. Also by the mid 1970’s work on self-control, also with its

roots in behaviour analysis [36] was incorporated into the treatment armamentarium

5
and a definitive text ‘Pain and behavioral medicine: a cognitive-behavioral perspective’

[63] was published in 1983.

At the turn of the 1970s Beck published a text on the treatment of depression

by cognitive therapy [4]. The significance of this was that a substantive claim was

made that a disorder that had previously been difficult to treat using psychological

methods was treatable. Beck and Ellis had developed separate versions of what

became known as cognitive therapy in the previous two decades. The treatment was

grounded in acute clinical observation and a willingness to devise and test treatment

tactics in a clinical setting, rather than fundamental laboratory experimentation.

Cognitive therapy emphasized the critical meditational role played by idiosyncratic

interpretations of events in determining a person’s emotional and behavioural

responses to event. The model included a structural analysis of dysfunctional

thinking and hypothesized the development of underlying schema and modes of

information processing. Experimental analyses of elements of cognitive therapy

emerged in conjunction with later randomized controlled trials of Beck’s therapy.

Perhaps because of the marked overlap between pain and depression elements of

Beck’s therapy were incorporated into pain treatments and the model was adapted

to the treatment of chronic pain [59].

A second strand of treatment without roots in experimental psychology,

mindfulness, was also introduced in the mid-1980s. Kabat-Zinn [28] reported

uncontrolled evaluations of the application of mindfulness training derived from

6
Buddhist teaching and 3000 years of practice. Although Kabat-Zinn reported studies

on pain patients it was not until his work was taken up by a group of researchers

looking for a method to prevent relapse after treatment for depression [58] that

mindfulness was incorporated more generally into CBT.

The final strand of current CBT is the application of the generalized fear-

avoidance model to chronic pain. The modern experimental and clinical analysis of

fear and avoidance has a long history dating to the work of Masserman, Miller and

Mowrer in the 1940s. This work shaped the development of behavioural treatments

of phobias. Fordyce noted the importance of avoidance but the contemporary

analysis and application to chronic pain was provided in a seminal paper by Vlaeyen

and Linton [66]. In contrast to other approaches the fear-avoidance model is

relatively specific and in its primary instantiation it applies to a subgroup of patients

who express fears that engaging in specified movements will result in catastrophic

consequences. Treatment proceeds by having patients test the validity of their

appraisals by engaging in the very behaviour of which they are frightened. In many

regards the fear-avoidance model captures the essence of CBT which is the careful

formulation of an individual’s problem followed by treatment that is devised to test

their assumptions and alternative ways of responding via individualized

behavioural experiments [5].

Interruption, Interference and Identity: A framework for the psychology of pain

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 The literature on the psychology of pain is extensive but much of it can be

subsumed under three interlinked themes; interruption, interference, and identity

[42,44]. Interruption refers to the impact of pain on the disruption of attention and its

behavioural consequences on a moment-to-moment [15,32]. Continued disruption

has significant consequences for behavioural and cognitive performance [14,21]

resulting in interference so that a person fails either to complete tasks effectively or

performs them in a degraded manner that is unacceptable to them or members of

their social group. Repeated interference of key tasks impacts upon the person’s

sense of who they are and, perhaps more importantly, whom they might become by

distorting their vision of their future and reshaping their view of the past

[10,44,49,51,]. The importance of each theme varies across people and the duration

of pain. Brief laboratory pain has interruptive effects but unlikely to produce

interference or impact on identity. Acute clinical pain has both interruptive and

temporary interference effects but is unlikely to affect a person’s identity. Chronic

pain frequently has a profound effect on all three categories. Repeated interference

with tasks that are essential to achieving various life goals and maintaining a

person’s status in society impact on their sense of self and their future plans [43,57].

This brief analysis illustrates the breadth of disruption that pain may have on

normal psychological processes. The range of treatment procedures developed

within the cognitive-behavioural framework represents considered attempts to

8
relieve elements of suffering associated at each level of interruption, interference and

identity.

The tale of two RCTs: Evidence-Based Practice and Practice-Based Evidence

The distinction between efficacy and effectiveness in evidence-based practice1

is widely accepted. The major tool for building evidence is the randomised

controlled trial (RCT) and the strategy has been to establish evidence for the efficacy

of interventions using highly controlled RCTs, followed by effectiveness trials in

which the experimental constraints are relaxed so that the intervention can be tested

in routine practice. (In practice this distinction may be somewhat blurred.) The

evidence is summarised using systematic review and meta-analytic methodology

and disseminated to practitioners to implement in routine clinical treatment – the

second RCT. This framework describes a one-way pathway from laboratory to

routine implementation and essentially prioritises and privileges randomised

controlled trials, albeit with some justification, but perhaps to the neglect of evidence

generated in clinical practice [2]. Strategies for using data generated in routine

clinical practice to inform the evidence base for treatments have been relatively

lower on the clinical research agenda. Practice-based evidence generates a flow of

information from the clinic to basic research essentially ‘closing the loop’ and

providing an explicitly recursive approach to the evidence base. Practice-based

evidence is needed to validate the utility of interventions and improve the quality of

1
I have chosen to use ‘practice’ as it is a more generic term than ‘medicine’ and includes disciplines outside of
medicine that are sometimes rather disparagingly referred to as para-medical.

9
clinical practice. It may contribute new knowledge and items for the clinical research

agenda in its own right. The remainder of this article (1) illustrates the possible use

of RCTs to generate benchmarks for clinical practice; thereby providing the basis for

practice based evidence of a treatment, and (2) outlines two substantial issues

(measurement and treatment integrity) where evidence can be generated in practice

that can inform clinical trials.

The evidence base for CBT

The efficacy of CBT procedures has consistently been subjected to empirical

testing [24,16,45]. There is evidence for the absolute efficacy of CBT procedures i.e.

CBT is superior to no treatment and some suggestion that CBT may be marginally

superior on some measures compared with other treatments i.e. relative efficacy.

This overall conclusion should be placed in the context of the nature of the trials.

Arguably we can have most confidence in the results of a meta-analysis when all the

key parameters (samples, diagnoses, interventions, control arms, outcome measures

etc) are homogeneous. This is not the case with respect to CBT for chronic pain

where there is marked heterogeneity across all parameters which then have to be

aggregated [23]. While this is not ideal it does reflect the reality of this complex field

and it is reasonable to conclude that there is evidence for a class effect of CBT

procedures for a range of conditions where chronic pain is the significant feature.

Most outcome measures in these studies are continuous rather than categorical or

binary and the computed effect size is the standardised mean difference between the

10
treatment and control arms (Cohen’s d or Hedge’s g) [53], estimates of absolute

efficacy range from d = 0.2 to 0.5 [24,16,45].

Benchmarking: using the data from RCTs in clinical settings

Benchmarking refers to methods to methods which facility the development

and implementation of best practice. The methods are structured and rely on

metrics that enable one to compare the activity of routine clinical treatment with the

best available evidence and to develop and implement plans to improve current

performance levels where they fall short of best practice [2,33]. For example, data

from RCTs can be used to generate benchmarks to evaluate the effectiveness of

routine clinical treatment for particular service setting.

In the standard (non-benchmark) method evidence for the effectiveness for

CBT interventions in clinical practice primarily relies on the comparing pre and post

treatment measures of outcomes. It is possible to generate a range of statistics (%

change, mean difference, pre-post effect size) and to conduct inferential statistical

tests [47]. In the absence of an untreated control group it is difficult to evaluate

whether the observed changes are attributable to the intervention or other factors

that have occurred over the same period i.e. natural history. Minami and colleagues

have [40,41] developed a methodology using the estimates of the magnitude of pre-

to post-treatment (or pre-treatment to follow-up) change from both the treated and

control arms of RCTs. In essence a meta-analysis of relevant trials is conducted to

estimate the effect sizes and confidence intervals for change in the treated and

11
control arms. These statistics provide two benchmarks. The change in the untreated

group estimates change due the natural history of the disorder and the effects of

measurement and provides a benchmark for these effects (natural history

benchmark). The change in the treatment arm generates the benchmark for

treatment. The pre-post effect size of routine clinical treatment in a clinical service

setting can be computed and compared to the two benchmarks. The exact statistical

procedure provides certain safeguards and when implemented it is possible to

determine whether the service delivered in routine clinical treatment is within the

confidence intervals for the treatment benchmark or the natural history benchmark.

Fenton [18] conducted a proof of concept study for chronic pain. The omnibus

benchmarks for treated and natural history arms over all these trials are shown in

Figure 1. It is possible that routine clinical treatments in services may exceed these

benchmarks [67] when services pay detailed attention to the quality of treatment

implementation. The heterogeneity associated with the trial set used by Fenton

means that services should be cautious in using the omnibus estimates shown in

Figure 1. A better strategy would be to identify high quality trials where the format

and content of treatment closely matches that delivered by the service and the

measures used in the service correspond to those used in the trials.

FIGURE 1 HERE

The continuing saga of measurement - Challenge 1

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 There are three questions we might ask about the measures: (1) What should

we measure? (2) From whose perspective? and, (3) How much change is required?

What domains should be measured?

In trials of pharmacological and other medical interventions e.g. spinal cord

stimulation, the main aim is to modulate the sensory-intensity qualities of pain. The

primary endpoint is pain and measures of other domains are ancillary. The work of

IMMPACT [26,61] recommends measurement of particular domains e.g. physical

functioning, and specific measures within each domain, that cover many of the facets

of interest to trialists and patients, but it is premature to foreclose on particular

measures [39]. Different instantiations of CBT may legitimately lay claim to specific

outcomes and it is entirely consistent to incorporate additional specific measures e.g.

the fear-avoidance model requires assessment of specific avoidance behaviour.

Trialists and services might reasonably select robust generic measures, such as those

defined by IMMPACT, and specific measures that are consistent with the exact

model of therapy being given; indeed this is readily observable in many trials [31].

A nuanced evaluation of treatment depends on maintaining this distinction.

Whose perspective?

Although the majority of measures used in RCTs and clinical settings are

patient reported outcomes who defines what should be measured is rarely debated.

Measures are selected by researchers and clinicians on the grounds of relevance for

13
there particular intervention and their psychometric characteristics. For the most

part they are inherently sound but the content of what is assessed is biased by

privileging a single stakeholder, the researcher-clinician. Recently consideration has

been given to patients’ perspectives on the importance of outcomes. For example

IMMPACT [62] used mixed qualitative-quantitative methods to determine outcomes

considered important to patients. The results indicated that patients valued

improvements in sleep, cognitive function and social role engagement. While the

latter is often measured the former two are rarely incorporated in outcome

measurement. The addition of patient determined outcomes would be a valuable

addition to the evaluation of treatments in general.

How much a change?

The use of the effect size statistic to evaluate the outcome of CBT stems from

the preference of psychologists to construe and measure psychological variables as

continua. This deeply held assumption about the continuity of experience is

disadvantageous when patients and policy makers want yes/no answers to questions

e.g. ‘will this treatment relieve my pain?’ The advantage of the ES (d) statistic is its

capacity to provide a common metric across measures but its interpretation requires

attention to contextual features. Consider the two panels in Figure 2. Each panel

represents data from an RCT in which the initial scores are identical in each group.

At post treatment the ES = 0.5 (a medium effect size) in both trials and we might be

tempted to conclude that they are equivalent. Line C represents a cut-off score

14
denoting an interpretation which has clinical validity e.g. patients with scores below

the cut reduce their use of medication by a factor of 10. The interpretation of the of

the trial results is now entirely different and the treatment in trial B is markedly

preferable. The imposition of cut scores also makes the outcomes more

communicable to patients.

A potential disadvantage of the effect size relates to how one communicates

the effectiveness of treatment to patients. For an average effect size of d = 0.5 we can

say that after treatment the averaged treated person is at the 69th percentile of the

untreated control group. A degree of statistical literacy is required to interpret this

statement. The 69th percentile is probably meaningless to most patients, as it is not

referenced to a tangible behavioural marker such as ‘four out of 5 people who take this

treatment are able to do their own supermarket shopping’. One challenge is devise

methods of categorising change on continuous measures as behavioural referents

that have substantive clinical and social validity. Progress has been made in the

categorisation changes in pain and a consensus appears to be emerging that in many

settings a change of around 30% or a two point decrement on a 0-10 numerical rating

scale is perceived by patients as noticeable after treatment [17]. Devising categorical

outcome criteria also has the advantage over the effect size in that the outcome for

individual patients can also be documented.

FIGURE 2 HERE

15
 What change do chronic pain patients see as meeting their treatment

aspirations before treatment for other domains importance? [68] Robinson and

colleagues report two studies in which chronic pain patients were asked to make

ratings of their desired outcome on single items assessing pain, fatigue, distress and

interference [52]. In both studies the percentage decrement required exceeded 50%

and approached 70% in for the interference measure. In their second study patients

re-estimated their desired levels after 2 months of treatment and their estimates were

reduced by 10% to 15% [7] . Whether this represents an adjustment in expectations

following exposure to treatment or some methodological / measurement artefact is

not known. Thorne and Morley extended Robinson and colleagues’ work and used

standardised multi-item questionnaires with known psychometric properties [60].

This enabled them to use the statistical properties of the scales to generate other

summary data and to define categorical outcome using Jacobson’s reliable change

index (RCI) and clinically significant change (CSC) criteria to develop categorical

outcomes from the continuous scales [27]. The procedure is illustrated graphically in

Figure 3 in which the pre treatment and post treatment scores are plotted.

FIGURE 3 HERE

In this example improvement is indicated by a reduction in the score. The

line of no change is shown by the diagonal line. Knowledge of the scale’s reliability

and the variability of the sample are used to compute the magnitude of change that

can be regarded as reliable (RCI). A data point falling within the two dotted lines

16
parallel to the diagonal indicates that that person has not changed sufficiently for us

to discount the possibility that the change is measurement error. Points outside of

that indicate that the person has made a reliable change. We can now impose a

second criterion onto the scale by determining a cut point2. This is marked by the

vertical and horizontal lines (cross-hairs) on the plot defining patients who fall above

and below the cut point pre and post treatment. Figure 3 shows the various

categories that can be determined from this analysis. Thorne and Morley’s sample

reported desiring percent changes in the outcomes in the same range as Robinson’s

patients i.e. > 50%. The data were also analysed to produce effect size statistics and

these values ranged from 1.38 to 1.70, which are far in excess of values observed in

current RCTs. Finally, the proportion of patients whose scores met RCI and SCS

criteria were also computed. One consequence of this was that for some patients,

those who estimate that a small change would be satisfactory, the change is too small

to be reliably measured or to be regarded as clinically significant according to the

criteria used i.e. the measurement technology is insensitive to the patient’s criteria.

These studies have used prospective judgements made by chronic pain patients and

reveal the range of desired outcomes and expectations. The magnitude of the

expectation is often in excess of what can be delivered by current treatments and

understanding the implications of this discrepancy requires attention. Finally,

2
Jacobson described statistical criteria for determining cut points but they may also be determined by other
methods such as social (expert) consensus or the use of a ‘gold standard’ index and receiver operating curve
analysis.

17
Morley et al provide an example of the application of RCI/CSC methodology to

assess the outcome of routine treatment [47].

The quality of treatment: Challenge 2

The magnitude of the effect size is often interpreted in qualitative terms using

the categories popularised by Cohen [11]: 0.2 = small, 0.5 = medium, 0.8 large. The

fact that Cohen stressed that these qualitative interpretations were dependent on the

context of the study is sometimes forgotten. The effect size may also be considered

as a correlation [53] and interpreted as representing the magnitude of variance

explained in a bivariate relationship. In the context of an RCT the effect size between

treatment and control at the end of treatment represents the degree of variance in the

outcomes attributable to treatment. A typical effect size (d = 0.5) found in studies of

chronic pain indicates that around 6% of the variance in outcome measures is

attributable to the intervention. Analyses of psychotherapy studies provide an

estimate for the absolute efficacy of treatments at around d = 0.8, which is equivalent

to about 14% of the variance [71]. Butler [9] reviewed 16 meta-analysis of CBT for a

range of disorders and reported a weighted grand mean ES(d) = 0.95, or about 18.5%

of the variance. A naïve assumption might be that all of this variance is attributable

to the specific effects of treatment but more nuanced analyses indicate that much the

variance is attributable to other factors, such as the therapeutic alliance between

patients and therapists, the competence of the therapist, and their allegiance to the

specific therapeutic model [71]. There is little research on therapist effects in the

18
cognitive behavioural treatment of chronic pain. The analysis of studies has largely

ignored the effect of groups and variation in therapists [1] but evidence is emerging

that such effects are present and important [34,72] .

Unlike pharmacological treatments psychological treatments are entirely

manufactured by therapists at the point of delivery. Treatments are dynamic,

constructed ‘in the moment’ and subject to the influence of context such as the

individual patient or the group setting. Quality control of treatment therefore

resides in the training, supervision and guidance given to practitioners as well as

their own ability to reflect on and appraise their behaviour while conducting

therapy. The provision of manuals detailing the structure and content of therapy is

now a mandatory requirement for psychological treatments in clinical trials. In

addition it is generally expected that trial therapists undertake supervised training

cases and remain in supervision for the period of the trial. The quality scale

developed by Yates et al [74] captures some of these facets of treatment quality. The

scale was used to rate trials 66 trials of psychological therapy published between

1985 and 2009. The resulting analysis indicated that there was no discernable trend

across the 25 years that treatment quality as reported in the trials had significantly

improved. In contrast the design component of trials had significantly improved,

Figure 4. Borelli [6] also developed a measure of treatment fidelity that identifies

five components: Treatment design; training of therapists; delivery of treatment;

receipt of treatment; and enactment of treatment skills. The latter two explicitly

19
assess the patient’s uptake of the treatment and their active use of treatment

strategies. Borrelli examined of 342 trials of behavioural medicine published over a

period of 10 years and found that the mean proportion of adherence to treatment

fidelity strategies was around one half (0.55): Again there was no discernable

improvement over time. More recently Perepletchikova [50] examined treatment

integrity of psychosocial treatments for a range of problems and concluded that

‘investigations that systematically address treatment integrity procedures are

virtually absent in the literature’. A significant challenge is therefore to improve not

only the power of the specific technical aspects of interventions i.e. specific

behaviour experiments and behaviour change strategies, but to enhance the quality

of their implementation by practitioners.

FIGURE 4 HERE

The problem of quality assuring treatment is non-trivial in both research and

routine clinical treatment settings and requires significant investment and thought.

One established protocol [70] is illustrated by Leeuw’s analysis of a trial comparing a

fear-avoidance treatment protocol against a protocol for graded activity [30]. The

treatments were concept mapped to describe features that were: (i) essential and

unique; (ii) essential but not unique; (iii) unique but not essential; (iv) compatible but

neither essential nor unique; and (v), prohibited. Videotapes of treatment sessions

were acquired and rated by independent observers. An estimate of treatment

integrity can be derived and the degree to which contamination occurs is assessed by

20
the degree to which intrusions of therapeutic activity from categories (i) and (v) into

the target therapy. This very thorough procedure has disadvantages in that it is

costly and the full analysis can only be achieved after treatment is complete. This

makes it unsuitable for routine clinical use where rapid feedback and shaping of the

therapy is required. In addition the instantiation of pure treatment forms while

necessary for randomized clinical trials does not necessarily guarantee that

appropriate changes in the individual patient will occur. The dynamic nature of

treatment means that practitioners may change their therapeutic behaviour in

response to changes in the patient. These changes are not necessarily effective and

therapists may drift from known effective interventions especially when confronted

with problems and difficulties [69]. Treatments that require active behavioural

change may easily revert to mere talking: therapists take the line of least resistance.

Approaches that monitor outcomes or outcome indicators may have greater

applicability and utility in clinical settings. For example, Lambert and colleagues

[29] have reported studies in which an outcome assessment tool (the OC-45) has

been administered after each session. The establishment of a large database in which

patient progress was tracked during the course of therapy enabled Lambert to devise

the equivalent of a manufacturing control chart and to detect patients who failed to

respond within expected parameters. Lambert has demonstrated that provision of

feedback and clinical support tools both increased the number of patients making

21
reliable and clinically significant changes and decreased the proportion showing

deterioration.

Given the plethora of outcome measures in the field of chronic pain it may not

be possible to instigate an identical strategy but and alternative would be to identify

valid markers of the change process that could be used to track progress. There are

relatively few change process studies [46] given the volume of trials but several

recent ones [35, 55,56,64] and cohort studies [8] have begun to explore this issue. The

advent of daily diary methodology, including electronic diaries and automated

telephone contact [48], and the development of suitable statistical analysis (multi-

level modeling) provide a suite of tools that may help advance our understanding of

change. Possible indicators of good outcomes include changes in catastrophizing,

self-efficacy and control beliefs; all of which can be measured with relative ease. On

the other hand clinicians and researchers might adopt the ‘old’ technology of single

case experimentation [3,38]. Fordyce’s early studies were dependent on this

methodology and more recently Vlaeyen and his colleagues [13,65] have used

replicated single cases to establish the therapeutic potential of the fear-avoidance

model. The cardinal feature of behaviourally informed single case methodology is

that the target outcome measure may also be the process measure [54]. These

methods are readily implementable.

Summary

22
 CBT is a class of treatments that have developed over 50 years in response to

changing conceptualisations of pain and changing conceptualisations of

psychological change mechanisms. The psychology of chronic pain is extensive and

ranges from attention control and factors influencing performance of important

social roles to aspects of identity construction. A legitimate case can be made for

treatment intervention at any of these levels. To some extent theorists and clinicians

continue to struggle to articulate causal models that contain sufficient precision to be

subjected to unambiguous tests and facilitate the development of robust treatments

generating large magnitude changes. One danger is that each new conceptualisation

and therapeutic school that shows promise becomes diluted when implemented in

routine clinical practice as elements may simply be added into existing treatment

protocols. Treatment will undoubtedly continue to develop and as it does further

attention should be given to: (1) developing measures with robust criteria to index

meaningful clinical change in addition to statistical estimations of significance, and

(2) methods for assuring the integrity and quality of treatment implementation.

23
Acknowledgements

I owe a big debt of gratitude to many colleagues and collaborators over the

years. Particular thanks go to Amanda Williams, Chris Eccleston, Johan Vlaeyen,

Frank Keefe, Geert Crombez, Henry McQuay and Andrew Moore, and to my clinical

colleagues in the Leeds Pain Service. Several graduate students have collaborated in

research projects and I thank them for their diligence and generosity: Shona Yates,

Grania Fenton, Fiona Thorne and Sumerra Hussain, whose untimely death in the

summer of 2009 this manuscript commemorates

Conflict of interest and disclosure

No conflict of interest is declared. The author has received speaker’s fees

from Pfizer in the last 12 months.

24
References

1 Baldwin SA, Murray DM, Shadish WR. Empirically supported treatments or

type I errors? Problems with the analysis of data from group-administered

treatments. J Consult Clin Psychol 2005;73(5):924-935.

2 Barkham M, Hardy GE, Mellor-Clark J. Developing and delivering practice-

based evidence: a guide for psychological therapies. Chichester: Wiley-

Blackwell, 2010.

3 Barlow DH, Nock M, Hersen M. Single case experimental designs: Strategies

for studying behavior change. New York: Pearson, 2009.

4 Beck AT, Rush AJ, Shaw BF, Greenberg RL. Cognitive therapy of depression.

New York: Guilford Press, 1979.

5 Bennett-Levy J, Butler G, Fennell M, Hackman A, Mueller M, Westbrook D.

Oxford guide to behavioural experiments in cognitive therapy. Oxford:

Oxford University Press, 2004.

6 Borrelli B, Sepinwall D, Ernst D, Bellg AJ, Czajkowski S, Breger R,

DeFrancesco C, Levesque C, Sharp DL, Ogedegbe G, Resnick B, Orwig D. A

new tool to assess treatment fidelity and evaluation of treatment fidelity

across 10 years of health behavior research. J Consult Clin Psychol

2005;73(5):852-860.

25
7 Brown JL, Edwards PS, Atchison JW, Lafayette-Lucey A, Wittmer VT,

Robinson ME. Defining patient-centered, multidimensional success criteria

for treatment of chronic spine pain. Pain Med 2008;9(7):851-862.

8 Burns JW, Kubilus A, Bruehl S, Harden RN, Lofland K. Do changes in

cognitive factors influence outcome following multidisciplinary treatment for

chronic pain? A cross-lagged panel analysis. J Consult Clin Psychol

2003;71(1):81-91.

9 Butler AC, Chapman JE, Forman EM, Beck AT. The empirical status of

cognitive-behavioral therapy: A review of meta-analyses. Clin Psychol Rev

2006;26(1):17-31.

10 Charmaz K. From the "sick role" to stories of self: understanding the self in

illness. In: RJ Contrada, RD Ashmore, editors. Self, social identity, and

physical health, Vol. 2. Oxford: Oxford University Press, 1999. pp. 209-239.

11 Cohen J. Statistical Power Analysis for the Behavioral Sciences. New York:

Academic Press, 1977.

12 Dahl JC, Wilson KG, Luciano C, Hayes SC. Acceptance and commitment

therapy for chronic pain. Reno, NV: Context Press, 2005.

13 de Jong JR, Vangronsveld K, Peters ML, Goossens ME, Onghena P, Bulte I,

Vlaeyen JW. Reduction of pain-related fear and disability in post-traumatic

26
 neck pain: a replicated single-case experimental study of exposure in vivo. J

Pain 2008;9(12):1123-1134.

14 Dick BD, Rashiq S. Disruption of attention and working memory traces in

individuals with chronic pain. Anesthesia and Analgesia 2007;104:1223-1229.

15 Eccleston C, Crombez G. Pain demands attention: a cognitive-affective model

of the interruptive function of pain. Psychol Bull 1999;125(3):356-366.

16 Eccleston C, Williams ACdeC, Morley S. Psychological therapies for the

management of chronic pain (excluding headache) in adults. Cochrane

Database of Systematic Reviews 2009.

17 Farrar JT, Young JP, Jr., LaMoreaux L, Werth JL, Poole RM. Clinical

importance of changes in chronic pain intensity measured on an 11-point

numerical pain rating scale. Pain 2001;94(2):149-158.

18 Fenton G. Benchmarking outcomes for psychological treatments of chronic

pain. Unpublished Doctoral thesis, University of Leeds, 2010.

19 Fordyce WE. Behavioral methods for chronic pain and illness. St Louis:

Mosby, 1976.

20 Gatchel RJ, Peng YB, Peters ML, Fuchs PN, Turk DC. The biopsychosocial

approach to chronic pain: scientific advances and future directions. Psychol

Bull 2007;133(4):581-624.

27
21 Grisart J, Van der Linden M, Masquelier E. Controlled processes and

automaticity in memory functioning in fibromyalgia patients: relation with

emotional distress and hypervigilance. J Clin Exp Neuropsychol

2002;24(8):994-1009.

22 Hayes SC, Barnes-Holmes D, Roche B. Relational frame theory: A post-

Skinnerian account of human language and cognition. New York: Kluwer,

2001.

23 Higgins JPT, Green S. Cochrane handbook for systematic reviews of

interventions. Chichester: Wiley-Blackwell, 2008.

24 Hoffman BM, Papas RK, Chatkoff DK, Kerns RD. Meta-Analysis of

psychological interventions for chronic low back pain. Health Psychol

2007;26(1):1-9.

25 Holroyd KA, Penzien DB, Hursey KG, Tobin DL, Rogers L, Holm JE, Marcille

PJ, Hall JR, Chila AG. Change mechanisms in EMG biofeedback training:

cognitive changes underlying improvements in tension headache. J Consult

Clin Psychol 1984;52(6):1039-1053.

26 IMMPACT. The Initiative on Methods, Measurement, and Pain Assessment in

Clinical Trials. www.impact.org

28
27 Jacobson NS, Roberts LJ, Berns SB, McGlinchey JB. Methods for defining and

determining the clinical significance of treatment effects: Description,

application, and alternatives. J Consult Clin Psychol 1999;67(3):300-307.

28 Kabat-Zinn J. An outpatient program in behavioral medicine for chronic pain

patients based on the practice of mindfulness meditation: theoretical

considerations and preliminary results. General Hospital Psychiatry 1982:443-

447.

29 Lambert MJ, Hansen NB, Harmon SC. Outcome Questionnaire System (the

OQ system): Development and practical applications in healthcare settings.

In: M Barkham, GE Hardy, J Mellor-Clark, editors. Developing and delivering

practice based evidence: A guide for the psychological therapies. Chichester:

Wiley-Blackwell, 2010. pp. 141-154.

30 Leeuw M, Goossens ME, de Vet HC, Vlaeyen JW. The fidelity of treatment

delivery can be assessed in treatment outcome studies: a successful

illustration from behavioral medicine. J Clin Epid 2009;62(1):81-90.

31 Leeuw M, Goossens ME, van Breukelen GJ, de Jong JR, Heuts PH, Smeets RJ,

Koke AJ, Vlaeyen JW. Exposure in vivo versus operant graded activity in

chronic low back pain patients: results of a randomized controlled trial. Pain

2008;138(1):192-207.

29
32 Legrain V, Damme SV, Eccleston C, Davis KD, Seminowicz DA, Crombez G.

A neurocognitive model of attention to pain: Behavioral and neuroimaging

evidence. Pain 2009;144(3):230-232.

33 Leuger RL, Barkham M. Using benchmarks and benchmarking to improve

quality of practice and services. In: M Barkham, GE Hardy, J Mellor-Clark,

editors. Developing and Delivering Practice-Based Evidence. Chichester:

Wiley, 2010. pp. 223-256.

34 Lewis M, Morley S, van der Windt DAWM, Hay E, Jellema P, Dziedzica K,

Main CJ. Measuring practitioner/therapist effects in randomized trials of low

back pain and neck pain interventions in primary care settings. Euro J Pain in

press.

35 Litt MD, Shafer DM, Ibanez CR, Kreutzer DL, Tawfik-Yonkers Z. Momentary

pain and coping in temporomandibular disorder pain: Exploring mechanisms

of cognitive behavioral treatment for chronic pain. Pain 2010;151(1):110-116.

36 Mahoney MJ, Thoresen CE. Self-control: power to the person. Monterey:

Brooks/Cole Publishing Company, 1974.

37 McCracken LM. Contextual Cognitive-Behavioral Therapy for Chronic Pain,

Vol. 33 Seattle: IASP Press, 2005.

30
38 McMillan D, Morley S. Single-case quantitative methods. In: M Barkham, GE

Hardy, editors. Developing and delivering practice-based evidence: a guide

for psychological therapies. Chichester: Wiley, 2010.

39 McQuay H. Editorial: Consensus on outcome measures for chronic pain trials.

Pain 2005;113(1):1-2.

40 Minami T, Serlin RC, Wampold BE, Kircher JC, Brown G. Using clinical trials

to benchmark effects produced in clinical practice. Quality & Quantity:

International Journal of Methodology 2008;42(4):513-525.

41 Minami T, Wampold BE, Serlin RC, Kircher JC, Brown GS. Benchmarks for

psychotherapy efficacy in adult major depression. J Consult Clin Psychol

2007;75(2):232-243.

42 Morley S. Psychology of pain. Brit J Anaesthesia 2008;101(1):25-31.

43 Morley S, Davies C, Barton S. Possible selves in chronic pain: self-pain

enmeshment, adjustment and acceptance. Pain 2005;115(1-2):84-94.

44 Morley S, Eccleston C. The object of fear in pain. In: GJ Asmundson, J

Vlaeyen, G Crombez, editors. Understanding and treating fear of pain.

Oxford: Oxford University Press, 2004. pp. 163-188.

45 Morley S, Eccleston C, Williams A. Systematic review and meta-analysis of

randomized controlled trials of cognitive behaviour therapy and behaviour

therapy for chronic pain in adults, excluding headache. Pain 1999;80(1-2):1-13.

31
46 Morley S, Keefe FJ. Editorial: Getting a handle on process and change in CBT

for chronic pain. Pain 2007;127(2):197-198.

47 Morley S, Williams ACdeC, Hussain S. Estimating the clinical effectiveness of

cognitive behavioural therapy in the clinic: Evaluation of a CBT informed

pain management programme. Pain 2008;137(3):670-680.

48 Naylor MR, Keefe FJ, Brigidi B, Naud S, Helzer JE. Therapeutic Interactive

Voice Response for chronic pain reduction and relapse prevention. Pain

2008;134(3):335-345.

49 Osborn M, Smith JA. The personal experience of chronic benign lower back

pain: An interpretative phenomenological analysis. Brit J Health Psychol

1998;3(Part 1):65-83.

50 Perepletchikova F, Treat TA, Kazdin AE. Treatment integrity in

psychotherapy research: Analysis of the studies and examination of the

associated factors. J Consult Clin Psychol 2007;75(6):829-841.

51 Risdon A, Eccleston C, Crombez G, McCracken L. How can we learn to live

with pain? A Q-methodological analysis of the diverse understandings of

acceptance of chronic pain. Soc Sci Med 2003;56(2):375-386.

52 Robinson ME, Brown JL, George SZ, Edwards PS, Atchison JW, Hirsh AT,

Waxenberg LB, Wittmer V, Fillingim RB. Multidimensional success criteria

32
 and expectations for treatment of chronic pain: the patient perspective. Pain

Med 2005;6(5):336-345.

53 Rosenthal R. Parametric measures of effect size. In: H Cooper, LV Hedges,

editors. The handbook of research synthesis. New York: Russell Sage

Foundation, 1994. pp. 231-244.

54 Sidman M. The tactics of scientific research. New York: Basic Books, 1960.

55 Smeets RJEM, Vlaeyen JWS, Kester ADM, Knottnerus JA. Reduction of pain

catastrophizing mediates the outcome of both physical and cognitive-

behavioral treatment in chronic low back pain. J Pain 2006;7(4):261-271.

56 Spinhoven P, Ter Kuile M, Kole-Snijders AM, Hutten Mansfeld M, Den

Ouden DJ, Vlaeyen JW. Catastrophizing and internal pain control as

mediators of outcome in the multidisciplinary treatment of chronic low back

pain. Euro J Pain 2004;8(3):211-219.

57 Sutherland R, Morley S. Self-pain enmeshment: Future possible selves,

sociotropy, autonomy and adjustment to chronic pain. Pain 2008;137(2):366-

377.

58 Teasdale JD, Segal Z, Williams JMG. How does cognitive therapy prevent

depressive relapse and why attentional control (mindfulness) training help?

Behav Res Ther 1995;33(1):25-39.

33
59 Thorn BE. Cognitive therapy for chronic pain. New York: Guilford Press,

2004.

60 Thorne FM, Morley S. Prospective judgments of acceptable outcomes for pain,

interference and activity: Patient-determined outcome criteria. Pain

2009;144(2/3):262-269.

61 Turk DC, Dworkin RH, Allen RR, Bellamy N, Brandenburg N, Carr DB,

Cleeland C, Dionne R, Farrar JT, Galer BS. Core outcome domains for chronic

pain clinical trials: IMMPACT recommendations. Pain 2003;106(3):337-345.

62 Turk DC, Dworkin RH, Revicki D, Harding G, Burke LB, Cella D, Cleeland

CS, Cowan P, Farrar JT, Hertz S, Max MB, Rappaport BA. Identifying

important outcome domains for chronic pain clinical trials: An IMMPACT

survey of people with pain. Pain 2008;137(2):276-285.

63 Turk DC, Meichenbaum D, Genest M. Pain and behavioral medicine: a

cognitive-behavioral perspective. New York: Guilford Press, 1983.

64 Turner JA, Holtzman S, Mancl L. Mediators, moderators, and predictors of

therapeutic change in cognitive-behavioral therapy for chronic pain. Pain

2007;127(3):276-286.

65 Vlaeyen JW, de Jong J, Geilen M, Heuts PH, van Breukelen G. Graded

exposure in vivo in the treatment of pain-related fear: a replicated single-case

34
 experimental design in four patients with chronic low back pain. Behav Res

Ther 2001;39(2):151-166.

66 Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences in chronic

musculoskeletal pain: a state of the art. Pain 2000;85(3):317-332.

67 Vowles KE, McCracken LM. Acceptance and values-based action in chronic

pain: A study of treatment effectiveness and process. J Consult Clin Psychol

2008;76(3):397-407.

68 Vowles KE, Robinson ME. Progressing towards acceptable treatment

outcomes. Pain 2009;144(3):228-229.

69 Waller G. Evidence-based treatment and therapist drift. Behav Res Ther

2009;47(2):119-127.

70 Waltz J, Addis ME, Koerner K, Jacobson NS. Testing the integrity of a

psychotherapy protocol: Assessment of adherence and competence. J Consult

Clin Psychol 1993;61(4):620-630.

71 Wampold BE. The great psychotherapy debate: Models, methods, and

findings. Mahwah, NJ: Lawrence Erlbaum Associates, 2001.

72 Williams ACdeC, Potts HW. Group membership and staff turnover affect

outcomes in group CBT for persistent pain. Pain 2010;148(3):481-486.

35
73 Williams ACdeC. Cognitive-behavioural pain management: lessons learned.

In: H McQuay, EA Kalso, RA Moore, editors. Systematic reviews in pain

research: Methodology refined. Seattle: IASP Press, 2008. pp. 275-284.

74 Yates S, Morley S, Eccleston C, Williams ACdeC. A scale for rating the quality

of trials of psychological trials for pain. Pain 2005;117(314-325).

36
 FIGURES

Figure 1

This figure shows omnibus effect size (d) benchmarks with 95%CIs for CBT (solid)
and waiting list control (open) averaged pre-post treatment changes in randomised
controlled trials for five domains. Data from [18].

37
Figure 2

The two panels in this figure represent idealised pre- to post-treatment changes on
an outcome in two trials, A and B. Each trial has two arms, a control (solid line) and
treatment (dashed line), and the mean at the start of treatment for is identical across
arms and trials. An improvement is indicated by a decrease in the measure. At the
end of treatment difference between the treated and control arms in both trials is
identical and has an effect size [ES(d) = 0.5]; the distribution of the scores shown by
the normal curve for each arm. If the ES(d) values are considered trial A and B are
identical in there effect. If however we have an established cut point denoting the
boundary for a clinically significant change it is clear that very few people in trial A
meet this criterion whereas most people in the treatment arm of trial B may be
regarded as clinically improved.

38
Figure 3

This figure is a tramline display in which the data from individual patients at pre-
treatment (x-axis) and post-treatment (y-axis) are plotted. For a patient who has the
same score on both occasions i.e. no change in score, the data point will fall on the
main diagonal axis (solid line). Any point that is not on the main diagonal indicates
some change. Other information plotted on the display enables us to judge the
significance of the change. The parallel lines either side of the main diagonal are the
95% confidence intervals for the error of measurement and any data point that falls
between these lines is not significantly different from the main diagonal i.e. no
significant change has occurred. Data points outside the confidence interval mean
that the person’s score has reliably changed. Note that this enables us to detect both
reliable improvement and deterioration.
The vertical and horizontal dotted lines plotted for values of x and y = 20
indicate a clinically meaningful cut score on the scale. Patients to the right of the
pre-treatment (vertical) cut score were above the clinical criterion at pre-treatment.
Patients below post-treatment cut score (horizontal) were below the clinical criterion
at post-treatment. As a result we can now classify individual patients on the
additional criterion of whether they have made a significant clinical improvement.
Note that patients below the cut score at the start of treatment may make a clinically
significant deterioration.

39
Figure 4

Plot of ratings for two components of trial quality, study design (circles) and
implementation of treatment (triangles) for 66 trials of psychological treatment for
chronic pain published between 1984 and 2010 based on [16]. Regression analyses
indicate that whereas the design features of trials have improved over time the
reported implementation of treatment has not.

40
Table 1

Timeline outlining the development of CBT applied to the treatment of chronic pain.

The main schools are shown in bold face and their antecedents in italic.

1940 1950 1960 1970 1980 1990 2000

Operant
Behaviour
Operant
Analysis

Operant
Behaviour
Biofeedback
Analysis

1. Cognitive theory
of stress
2. Behavioural Stress
Analysis of self management
control

Clinical observations Cognitive

therapy

Buddhism Mindfulness
(1000 BCE) based stress
reduction

Mower-Miller Fear
2- process Avoidance
theory

Operant Behaviour Acceptance and

Behaviour analysis of Commitment
Analysis language therapy

41