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The Journal of Pain, Vol 17, No 5 (May), 2016: pp 529.e1-529.e18Available online at www.jpain.org and www.sciencedirect.com

Focus ArticleOnline Exclusive

The Behavioral Activation and Inhibition Systems: Implications for

Understanding and Treating Chronic Pain

Mark P. Jensen,* Dawn M. Ehde,* and Melissa A. Dayy

*Department of Rehabilitation Medicine, University of Washington, Seattle, Washington.ySchool of Psychology, University of Queensland, Brisbane, Queensland, Australia.

The authAddressRehabilitWashingmjensen

1526-590

ª 2016 b

http://dx

Abstract: Evidence from a number of sources supports the existence of two relatively independent

neurophysiological systems that underlie avoidance- and approach-related emotions, cognitions, and

behavior. There is considerable overlap between 1) the emotions, cognitions, and behaviors

controlled by these two systems, and 2) the known effects of chronic pain. Here we propose a

2-factor model of chronic pain on the basis of these well established 2-factor models, and discuss

the implications of the model for understanding the effects of pain and mechanisms of psychological

pain treatments. The model makes specific hypotheses, which are unique to the proposed model,

regarding the mechanisms underlying pain’s negative influence and the benefits of psychological

pain treatments. The model also provides an overarching framework that could enhance outcomes

by 1) broadening the assessment of factors that may be influencing pain and its effect on individual

patients, and 2) suggesting that specific techniques from different treatments may be combined to

better target these factors.

Perspective: The 2-factor model presented in this report provides a framework for understanding

the effects of psychological pain treatments, and makes specific a priori hypotheses regarding the

specific mechanisms of those treatments. Clinical applications of the model have the potential for

enhancing treatment outcomes.

ª 2016 by the American Pain Society

Key words: Behavioral inhibition system, behavioral activation system, chronic pain, theory,

mechanisms.

One of the most significant problems resultingfrom chronic pain—if not the most significantproblem—is its negative effect on psychological

and physical functioning. The presence and the severityof chronic pain are associated with depression,47,106

anxiety,5,71 and physical disability.64 Pain often interruptsbehavior34,44 and hinders progress toward valuedgoals.1,33 For some individuals, efforts to manage painand its effect become the central focus of their lives,

ors have no conflicts of interest to declare.reprint requests to Mark P. Jensen, PhD, Department ofation Medicine, Harborview Medical Center, University ofton, 325 Ninth Avenue, Box 359612, Seattle, WA 98104. E-mail:@uw.edu

0/$36.00

y the American Pain Society

.doi.org/10.1016/j.jpain.2016.02.001

severely limiting the time and energy available toengage in meaningful activities. As a consequence,chronic pain results in a marked decrease in the overallquality of life for many individuals.64 To develop themost efficacious treatments for helping people bettermanage pain’s effect on function and quality of life, itis important to understand the processes that underliepain’s influence on valued, goal-directed behavior.Over the past several decades, a number of models of

behavior, motivation, and emotion have been proposedthat hypothesize the existence of 2 distinct neurophysio-logical systems: one system underlying ‘‘approachbehaviors’’ and a second system underlying ‘‘avoidancebehaviors.’’24,32,36,40,50-52,57,80,81,134,135 Although theseare not the only neurophysiological systems thatcontrol or underlie all human behavior, they arehypothesized to play an important role in influencing

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529.e2 The Journal of Pain BIS-BAS and Pain

many of our emotional, cognitive, and behavioralresponses to environmental and sensory cues; inparticular, our decision(s) to inhibit behavior or toremain active. This article explores how a 2-factorneurophysiological model of approach and avoidancebehavior may 1) help us understand the effect of chronicpain on physical and psychological dysfunction, and2) explain how theoretically diverse psychosocial paininterventions have their beneficial effects.The article is organized into 6 sections. In the first

section, we present basic background informationabout, and briefly summarize the empirical support for,the 2-factor neurophysiological models of approachand avoidance behavior. Next, we propose and describethe key features of a 2-factor model of chronic painthat incorporates the basic tenets of these models. Inthe third section, we discuss how the proposed modelmay help us understand currently unresolved questionsconcerning 1) the effect of pain on activity, 2) the pur-pose and automaticity of pain-related catastrophizing,and 3) the mechanisms of different psychosocialpain treatments. In the fourth section, we describe anumber of key testable hypotheses derived from themodel. We then discuss the potential benefits of anoverarching model of psychosocial pain treatment,such as the one proposed. In the sixth and final section,we discuss some of the limitations of the model andsuggest directions for research to test and develop itfurther.

Two-Factor Models of BehavioralRegulation, Motivation, and EmotionA number of models and theories propose the

existence of 2 distinct neurophysiological systems thatunderlie behavioral regulation, motivation, andemotion.24,32,36,40,50-52,54,57,80,81,134,135 These modelswere developed by different research groups usingvarious methodological approaches, such as factoranalyses of measures of emotions134,135 andobservation of the effects of chemicals on animalbehavior.52 Although different in their methodologicalapproaches, the scientists who developed these modelsindependently came to the same general conclusion:there are 2 key neurophysiological systems that underliemany of the core elements of day-to-day humanbehavior and experience. The first is an approach systemresponsible for approach behaviors, associated emotions(eg, hope, joy, excitement, anger), and cognitive content(eg, self-efficacy). The second is an avoidance systemresponsible for behavioral withdrawal, associatedemotions (eg, anxiety, depression), and cognitivecontent (eg, threat attributions, hopelessness). These 2systems share similar cognitive processess—that is, theyare both influenced primarily by associative and experi-ential learning. They are also ‘‘automatic’’ in that theyoperate separately from executive control. Moreover, akey principal of these models is that the 2 subsystemsare relatively independent, in much the same way thatan acceleration system (controlled by the gas pedal)

and a braking system (controlled by the brake pedal)independently influence the speed of an automobile.We discuss research supporting this independency laterin this section.Probably the most often cited of the numerous

2-factor approach-avoidance models is Jeffrey Gray’sreinforcement sensitivity theory.50-52,54 This modelhypothesizes that the approach and avoidancesystems are activated when there are environmentalcues that signal the possibility of reward orpunishment, respectively. According to Gray’s model, inthe presence of cues that the organism has learned toassociate with reward, a behavioral approach system(BAS; also referred to as a behavioral activationsystem41) is activated, which then facilitates andencourages approach-related behaviors, cognitions,and emotions.What is rewarding, of course, varies from person to

person, and depends on the individual’s physiologicalstate (eg, Is the individual hungry or fatigued?), values(eg, the relative importance to the individual of specificactivities, such as paid employment, contributing to ahousehold, or socializing with friends), as well as thespecific goal(s) that the individual is focusing on at anyone point in time (eg, higher-level goals of ‘‘being agood person’’ vs somewhat lower-level goals such as‘‘being on time’’ vs the lowest-level goals representingspecific behaviors such as eating).18 As the individualbecomes aware of a discrepancy between a goal (eg, toeat food) and one’s current state (eg, being hungry andcurrently not eating), the BAS becomes activated.When the BAS is activated, the BAS-related cognitions,emotions, and behaviors all work together to increasethe likelihood that the potential reinforcement willactually occur.50

When one goal is achieved (eg, being hungry and theneating a satisfying, reinforcing meal), an individualwould then begin to behave in ways that addressanother goal. This next goal would be a BAS-relatedgoal if there are environmental cues that signal thepossibility additional rewards. Which goal one selects isdetermined by an interaction between the cue(s)focused on, evaluation of the importance of thepotential rewards that the cues signal (value), andexpectations that the reward will occur.38 BASactivation that facilitates access to the reward continuesuntil 1) the discrepancy between one’s current state andthe goal to experience the reward is reduced oreliminated (which is hypothesized to be associatedwith positive affect18), 2) another discrepancy becomesmore salient (eg, a cue suggesting the possibility ofa new and more valued reward presents itself), or3) attention is shifted to the possibility of punishment(by the emergence of a cue signaling this possibility),which interrupts the process and activates the behavioralinhibition system (BIS; see next paragraph). Thus, BISand BAS activation, and the behaviors, thoughts,and feelings that follow, is a dynamic, multifacetedprocess.16,17

In contrast, a separate BIS is hypothesized to becomeactivated in the presence of cues indicating the

Jensen, Ehde, and Day The Journal of Pain 529.e3

possibility or likelihood of punishment. Cues suggest-ing the possibility of punishment therefore create adiscrepancy between an ideal state (eg, safety,comfort) and the perceived possibility of an aversivestate (eg, physical damage, pain). This discrepancyactivates BIS, and could potentially override anyattention that is being paid to BAS-related goals.When the BIS is activated, behavior is interrupted,which allows the individual to determine the stepsthat might be necessary to avoid or manage theanticipated aversive stimuli; BIS activation causes aperson to ‘‘stop, look, and listen.’’49

In addition to the behavioral correlates of BISactivation—an interruption of ongoing behavior orwithdrawal—BIS-related cognitive and emotionalresponses also occur. Specifically, in conditions of BISactivation, the individual becomes more sensitive tosigns of potential danger or harm. Concomitantemotions that facilitate behavioral inhibition andhypervigilance, such as anxiety and feelings of hopeless-ness and helplessness, are initiated and facilitated.Importantly, when activated in the appropriate context,the BIS system is adaptive; as a result of the avoidance-oriented behavioral, cognitive, and emotional responsesfacilitated by BIS, stimuli that are potentially punishingare more likely to be avoided.Importantly, the model does not hypothesize that

environmental cues that activate the BIS/BAS areinherently good or bad. There are likely some(limited) cues that are ‘‘hard-wired’’ to elicit BIS orBAS activation in many if not most individuals(eg, snakes, spiders, heights, and pain as cues thatmay activate BIS; the presence of food [whensomeone is hungry] as a cue that may activateBAS). However, whether or not a specific cue willelicit BIS or BAS will vary from individual toindividual and is influenced by their learning historyas well as by their focus of attention, which can beinfluenced by the behavior of others. The capacityfor an individual’s learning history and focus ofattention to influence whether (and how much) BISor BAS are activated in the presence of pain is acentral idea underlying this article and the model itproposes; importantly, the likelihood of BIS or BASactivation can be changed.Much of the research examining individual differences

and the relative effects and influences of the behavioralactivation and inhibition systems in humans has usedCarver and White’s BIS/BAS scale.18 This scale wasdesigned to measure a person’s self-reported traittendency to respond to cues indicating the possibilityof punishment (BIS activation) and tendency to respondto cues indicating the possibility of reward (BASactivation). Factor analyses of the items from the BIS/BAS scale yield 4-factor solutions, with the BIS itemsloading on a single scale, and the BAS items loading on3 scales labeled reward responsiveness, drive, andfun-seeking. However, the 3 BAS subscales load stronglyon a single second-order factor (all loadings >.75),whereas the BIS scale loads strongly on its own second-order factor (loading = .93)—consistent with the idea

that the 3 BAS subscales form a cluster that is distinctfrom the BIS scale.18 Further, the BIS/BAS scale itemsreflect behavioral responses, cognitive content, andemotional responses that are unique to each system.This is consistent with the ideas that 1) the BIS and theBAS underlie responses in all 3 of these domains, and 2)these responses are linked together within the BIS orBAS system, and also that the 2 systems are relativelyindependent from each other. So although the emotionof anxiety is not the same thing as beliefs about a futurewith negative outcomes, and these are not the same asthe behavior of withdrawal, measures of these 3domains (anxiety, negative outcome expectancies,withdrawal behavior) tend to cluster together.Moreover, these domains are hypothesized to clustertogether, separately and distinctly, from a secondcluster made up of measures that assess positivevalence emotions such as joy and excitement, beliefsabout a future with positive outcomes, and approachbehavior.Research using the BIS/BAS scale provides evidence

consistent with Gray’s BIS-BAS model. For example, theBIS/BAS subscales have been shown to be associatedsignificantly with psychological disorders that areassociated with disruptions in emotional and behavioraldysregulation, such as compulsive gambling,7 manic-depressive disorder,3,55 and problem drinking,56 amongothers.9 Moreover, a great deal of evidence supportsthe conclusion that the BIS and BAS represent distinctsystems that facilitate avoidance and approachbehaviors, thoughts, and emotions, and are not merely2 sides of the same coin. For example, evidence fromfunctional magnetic resonance imaging studies indicatesthat the 2 systems involve different underlying neuro-physiological networks,29,74,76,82,99,117 as hypothesizedby Gray’s model; the amygdala has been shown asimportant to the detection of threat and theexperience of associated anxiety, whereas the basalganglia has been implicated as important to thedetection of reward.82,99

Further evidence for the presence of distinct BIS andBAS neurophysiological networks comes from electroen-cephalography research, which has found that scoresfrom a self-report measure of BIS and BAS activation(the BIS/BAS scale18) are associated with resting prefron-tal brain activity asymmetry; BIS has been reported tobe more strongly associated with greater relativeactivation in the right frontal brain area than the left,and BAS with greater relative activation in the leftfrontal region than the right.58,122 This is alsoconsistent with electroencephalography researchindicating that the left and right prefrontal areasprocess different emotional states. Greater activity inleft prefrontal brain areas is associated with‘‘approach’’ emotions (such as happiness and anger),and greater activity in right prefrontal brain areas isassociated with ‘‘withdrawal’’ emotions (such as anxietyand sadness).23,24,57,59

Although the BIS and BAS are punishment- andreward-oriented systems that differ with respect to theirspecificity versus global nature, both are adaptive and


essential to optimal functioning. Continuing with theautomobilemetaphor, to drive safely, one needs an auto-mobile that has a well functioning acceleration system(including the engine, transmission, and fuel system)and—perhaps even more importantly—a well func-tioning braking system. One needs to also know whento accelerate and when to brake in the right context.An automobile with a very powerful engine and thatdoes not have effective brakes, especially if it is beingdriven by someone with a tendency to drive fast andavoid the use of brakes, is more likely to have accidents.Similarly, an automobile that cannot go faster than 10miles per hour being driven by someone who brakes atany hint of possible danger, is not likely to make muchforward progress. Critically, to function well, peopleneed to know when to go or speed up, and also whento slow down or stop.

A 2-Factor BIS-BAS Model of Chronic PainThe parallels between the behavioral, cognitive, and

emotional responses commonly observed in individualswith chronic pain and the responses associated with BISand BAS activation are readily apparent. First, becausepain is experienced as aversive by most individuals, aBIS-BAS model of chronic pain would hypothesize thatpain and the cues that come to be associated with in-creases in pain would tend to activate the BIS. Forexample, if an individual has a pain condition in whichspecific activities are associated with an increase inpain, then engaging in those activities (or even thoughtsof engaging in those activities) would be hypothesizedto activate the BIS. This BIS activation would thenfacilitate behavioral inhibition (eg, inactivity or aninterruption of behavior), negative cognitive processesand content (eg, catastrophizing), and negative mood(especially fear and anxiety). Consistent with this idea,a wealth of research supports pain’s inhibitory effectson behavior,34 and a plethora of studies have foundpositive associations between measures of pain andnegative cognitive processes and content (eg,catastrophizing121) and between pain and anxiety.71,87

In addition, the presence of anxiety (an emotionalresponse hypothesized to be BIS-related) is associatedwith a tendency to focus more on threat-related cuesthan neutral cues, and also to impair disengagementfrom threat-related cues.77 In support of this idea,research shows that cues that signal the occurrence ofpain are more likely to increase the focus of attentionon that cue, relative to ‘‘safety cues,’’ which signal alack of pain.129

According to a BIS-BAS model of chronic pain, anincrease in pain or the presence of cues indicating thatpain will increase would not typically be expected tohave a direct effect on the BAS, because the BAS isactivated in the presence of cues signaling reward, notpunishment. However, because many of the BAS-related responses (approach behavior, positive mood,hope) are inconsistent with BIS-related responses(behavioral inhibition, negative mood, hopelessness),when BIS is activated in the presence or anticipation of

pain, a concurrent decrease in BAS activation could bepredicted. This idea is consistent with evidence that theBIS and BAS are somewhat mutually inhibitory—moreBIS activation tends to suppress BAS activation to somedegree and vice versa21—although activation withinone system does not completely disrupt the other.Thus, the presence and severity of pain could potentiallyhave an indirect (negative) effect on BAS activity via itseffects on BIS, because BIS has some inhibitory influenceon the BAS. Concurrently, predicted or experienced relieffrom pain typically entails a reward value and may leadto BAS activation, although this motivational/rewardvalue circuitry associated with pain cessation has beenfound to be disrupted in individuals experiencingchronic pain.4

Fig 1 provides a graphic representation of our firstformulation of a BIS-BAS model of chronic pain. Thismodel represents a combination of a 2-factor version ofthe model of chronic pain first published in 201169 anda more recent revision of that model.26 An importantcomponent of the previous framework of chronic painwas a hypothesized role for different brain states asinfluencing and moderating the effects of pain-relatedbehaviors, cognitions, cognitive processes, and emo-tions.26,69 In the 2-factor model proposed in this article,we highlight BIS and BAS activation as 2 potential ‘‘brainstates’’ that could underlie and facilitate specific classesof behavioral responses, cognitive content, andemotional responses in the context of chronic pain. Ofcourse, as mentioned previously and as discussed inmore detail later in the Limitations section of this article,the BIS and BAS are not the only brain systems thatinfluence behavior. However, the growing literaturefrom independent research groups that supports theprimacy of behavioral inhibition and activation systemssupports the explanatory power of binary models suchas the one proposed in this article.A number of important ideas and hypotheses related

to this model are worth emphasizing. First, unlikemany biopsychosocial models of chronic pain thathypothesize fairly specific unidirectional causal path-ways between the factors (eg, proposing that factor Acauses factor B, which then influences factor C, etc.),the BIS-BAS model proposed in this article hypothesizesand emphasizes mutual causation among the factors.For example, the fear-avoidance model hypothesizes a‘‘vicious cycle’’ of causation in the development ofpain-related disability, starting with the experience ofpain and the evaluation that this pain may indicateinjury.6,22,132 Alarming or catastrophizing beliefs aboutanticipated further injury is then thought to lead tofear of movement, which results in behavioralinhibition (ie, less movement and disuse), which thenleads to physical and mental deconditioning, whichitself can contribute to more pain, initiating the wholecycle again. Note that although the hypothesizedeffects are cyclical, they are still described asunidirectional in that the circle is hypothesized to go in1 direction only.In the currently proposed BIS-BAS model, the key

domains of behavior, cognitive content, and emotions

Environmental Cues

BIS BASCogni ve Content (eg, Pain =

Danger, An cipate punishment)Cogni ve Content (eg, Hurt ≠

Harm, An cipate reward)

Emo on and affect (eg, Anxiety, Depression)

Emo on and affect (eg, Excitement, Hope)

Behavior (eg, Avoid, “Stop, look, and listen”)

Behavior (eg, Approach, Goal-Directed)

(-)

Brain states

Cogni ve processes (eg, Automa c, Effortless, Associa ve)

Painpercep on

(-)(+)

Figure 1. A graphic representation of our first formulation of a BIS-BAS model of chronic pain.


are viewed from an interactional perspective, with eachone contributing to changes in all of the other factors,and without any one being central or primary. Insteadof causal connections indicating specific (and uni-) direc-tional paths from one factor to another, we envision thefactors within each of the BIS and BAS as beingassociated with each other in a type of ‘‘web.’’ From aclinical perspective, this means that behaviors, thoughts,and emotions may be viewed as mechanisms and also asoutcomes. Again, this model broadens our view. Forexample, for the most part, measures of mood or affect(primarily, depression, but also anxiety) are used asoutcome variables in chronic pain clinical trials.2,96,100

However, in the proposed BIS-BAS model, affect canalso be viewed as a causal agent that influencescognitions and behavior (see also Fredrickson42). Thisopens up the possibility for more treatment options,including treatments that target positive affect as aprimary treatment mechanism.93

Within the cognition–emotion–behavior web, thereare probably individual differences; it is likely that somestrings (ie, mutual causal connections) that connect thenodes (ie, the specific behavioral, cognitive, andemotional factors) of the model are stronger than othersacross individuals, and it is possible that some directionsof causation are stronger than others. These individualdifferences may be due to temperamental (genetic) pre-dispositions, associative learning history, or more likely,both. For example, in a given individual, it is possiblethat beliefs about outcomes may influence behaviormore than the engagement in that behavior influencesbeliefs about outcomes. However, the model hypothe-sizes at least some bidirectional influence among all ofthe factors, considering the dependence of the modelon associative learning.

Although the BIS/BAS systems are hypothesized to bedistinct, in the currently proposed model, the BIS andBAS share similar cognitive processes, including thoseof automaticity and perceived effortlessness.73 Thus,we view the BIS and the BAS as 2 components of whathas been described as the ‘‘reflexive’’ brain system83

(which has also labeled the ‘‘intuition,’’73 ‘‘associa-tive,’’113 and ‘‘system 1’’116 system). Together, BIS andBAS exist to facilitate quick decision-making regardingthe most critical aspects of an environmental stimulus(ie, ‘‘Is it a potential source of reward or danger?’’) todetermine whether or not it should be attended to,and how to react. The ability to make very rapidjudgements (automatic ‘‘intuitive’’ judgements withouthaving to ‘‘think’’) about persons, places, and objectshas a great deal of survival value.42

However, the automatic (‘‘subconscious’’8) BIS-BASsystems are not governed by a central executive systemthat has deliberate or conscious control. Their automa-ticity, which serves the important purpose of makingthem adaptive and efficient, is also a vulnerability. Asthey learn by association (and not by thinking), theycan and do override and interfere with the moredeliberate systems that are under voluntary control.Thus, to purposefully and successfully ‘‘reprogram’’ theBIS and BAS systems, treatments need to first teachpatients strategies for disengaging from BIS and BASreactions; to respond less automatically. This disengage-ment helps make it easier for the patient to create newconnections and associations, which then result inautomatic responses that may better serve the patient’sgoals. Often, but not necessarily always, this may involveencouraging ongoing and repeated practice tostrengthen the connections and new learning. Thepurposeful and conscious practice of strategies to create


new BIS and BAS connections is discussed further whenwe examine current psychosocial pain treatments froma BIS-BAS perspective.In the proposed model, mutual influences between

pain, the BIS, and the BAS, are also hypothesized. Specif-ically, the presence of or increase in pain is hypothesizedto usually increase (we say ‘‘usually increase’’ herebecause, as we argue later, this effect of pain on BIScan be altered with treatment) BIS activity (directly)and decrease BAS activity (indirectly), and the sensationof pain itself may also be facilitated by BIS, or inhibitedby BAS activity. In Fig 1, the thicker arrow leading frompain to BIS, relative to that from BIS to pain and the ar-rows indicating mutual influence between BAS andpain, represent a hypothesized stronger direct effect ofpain on BIS activation. These relations are hypothesizedbased on the fact that pain is usually aversive,65 as wellas the strong evidence supporting pain’s tendency tointerrupt behavior.34

Thus, this is not an ‘‘everything is associated witheverything to the same degree’’ model. Rather, centralto themodel is the hypothesis that the BIS-related factorshave stronger effects on other BIS-related factors thanthe BAS-related factors, and vice versa. For example, pos-itive affect is hypothesized to have a stronger associationwith 1) approach behavior than with withdrawalbehavior, and 2) positive outcome expectancies thanwith catastrophizing. Similarly, negative affect is hypoth-esized to evidence the opposite pattern of associations(ie, more strongly associated with withdrawal behaviorand catastrophizing). Consistent with this idea, andone of the key findings that contributed to the initialdevelopment of 2-factor models, is the robust researchthat supports the idea that measures of ‘‘positive’’ emo-tions form a single overarching factor that is distinctfrom a factor comprised of ‘‘negative’’ emotions.108,134

The model presented in this article extends this idea todomains other than just emotions, specifically, toapproach- and withdrawal-related behaviors and cogni-tions. As we discuss in the next section, this central tenetof the model, if supported in future research, has criticalimplications for the treatment of chronic pain.Another aspect of the model proposed in this article is

that, although the BIS and BAS are hypothesized to havesome mutual inhibition effects, they can both be activeat the same time; an individual can feel, think, andsometimes act in ‘‘2 ways’’ about a goal (eg, a patientcan want to, and be afraid to, engage in physicalactivity). The relative activation of BIS versus BAS withrespect to the goal in question determines how theperson will ultimately act (and think and feel) aboutthat goal (eg, if excitement about a marriage prevails,the couple will go through with the marriage, whereasif anxiety prevails, one or the other may leave the futurespouse standing at the alter).The degree towhich each system is activated, as well as

the specific goal-directed behaviors that result from thisactivation, depends on the individual’s learning historywith respect to the environmental cues that are presentand the goal(s) that are activated (also referred to as‘‘current concerns’’75). Ultimately, though, the model

predicts that the relative activation of each systemis the final common pathway that influences theindividual’s emotions, cognitions, and behavior. Thus,and as discussed in more detail in the next section, tosuccessfully treat pain and pain-related disability, anintervention could 1) decrease BIS activation in responseto pain, 2) increase BAS activation with respect to valuedgoals, or 3) decrease BIS and also increase BAS activation.

Understanding Chronic Pain From aBIS-BAS Perspective: Strengths of theModelAlthough the BIS-BAS model of chronic pain we

propose does have some important limitations that arediscussed in the next section, we also believe that themodel has a great deal of explanatory power for under-standing the effects of pain on emotions, thoughts, andbehavior. In this section, we provide 2 examples of thisexplanatory power by discussing how themodel explainsand predicts 1) why some people have problems withactivity management, otherwise known as a pacingproblem,97,98 and 2) why some people with chronicpain catastrophize about pain despite the clearnegative effects of catastrophizing.11,121 We chose todiscuss these 2 responses (of the many we could havediscussed) because they are both viewed as centralresponses that contribute to dysfunction and aretherefore targeted by psychosocial pain treatments—activity management being targeted by operanttreatment39 and catastrophizing being targeted bycognitive therapy125 as well as treatments on the basisof the fear-avoidance model of chronic pain22—andalso because in our view the BIS-BAS model provides aunique way of understanding these responses thatillustrate its explanatory power. We then finish thissection by illustrating how the model provides a way oforganizing the key factors that influence psychosocialtreatment outcomes, and may therefore prove usefulfor developing methods for enhancing the efficacy ofexisting treatments and for better patient treatment–matching.

A BIS-BAS Understanding of ActivityManagement ProblemsIn the 2-factor models, the BIS and BAS are thought to

have trait and state qualities. People vary with respect totheir inherent tendency to respond to cues indicatingthreat or reward, and these tendencies contribute toeach individual’s personality.Tendencies for having either an overactive BIS or

overactive BAS could also lead to significant behavioralproblems in the context of chronic pain. Perhaps thepotential problems of having an overactive BIS aremost obvious. Such an individual would be expected tobe more fearful in general, more likely to interpretsensations as painful, and more likely to respond as ifthose sensations were an indication of danger (ie, havea trait tendency to catastrophize in response topain). At the extreme, someone with a strong trait


tendency for more BIS activation would be at risk tobecome markedly deactivated in response to pain. Suchindividuals are perhaps most aptly described by thefear-avoidance model of chronic pain.6,22,132

Having an overactive BAS could lead to a different setof activity management problems. Decades ago Fordycedescribed a subset of individuals with chronic pain whowould show repeated periods of ‘‘boom and bust’’behaviors that he hypothesized contributed to increasedpain and disability over time, because of the increasedrisk for pain flare-ups resulting from the muscle atrophycaused by the (usually increasingly longer periods) of theinactivity phase.39 From a BIS-BAS perspective, we wouldpredict that this type of pacing problem would be morelikely to develop in individuals with an inherent trait ortendency to have a very active BAS. This problem wouldbe exacerbated in someone who also has a relativelyinactive BIS. For such individuals, relative inactivity isexperienced as aversive, so they would tend to evidencehigh baseline levels of activity and other approachbehaviors. These are often the individuals who appearto have deep and seemingly endless reserves of energy:the marathon runners, the weekend warriors, and theso-called ‘‘workaholics.’’ If such individuals were tohave an injury or otherwise develop a pain problem,their higher-than-average baseline BAS activation couldfacilitate a tendency to remain very active in thepresence of mild to moderate pain, and only evidencepain-related behavioral inhibition when the pain (result-ing from overuse) becomes severe. Although a veryactive BAS coupled with an inactive BIS might beadaptive and useful in some situations (eg, just beforeor during a task that requires physical endurance forsuccess, such as a sports competition), individuals whoare not able to shift from BAS to BIS activationappropriately are at risk for ‘‘overdoing,’’ and experi-encing all of the negative outcomes of this behavioralpacing problem.On the basis of the proposed model, individuals with

trait excessive BAS or BIS would be less likely to havethe capacity to flexibly shift from one to the other asappropriate. At the extremes, BIS individuals would belikely to turn into ‘‘couch potatoes’’ and high catastroph-izers, and BAS individuals would be likely to evidence the‘‘boom or bust’’ pacing problem. Both types ofindividuals would be hypothesized to be vulnerable todevelop chronic pain after an injury, but for differentreasons. Longitudinal research could test thesehypotheses concerning trait levels of BIS or BAS activity(measured, for example, using the BIS/BAS scale, orperhaps using measures of the personality domains ofneuroticism and extraversion) as risk factors for thedevelopment and maintenance of chronic pain.

A BIS-BAS Understanding ofPain-Related CatastrophizingCatastrophizing has been defined as ‘‘.an exagger-

ated negative ‘mental set’ brought to bear duringactual or anticipated pain experience.’’121 pp 53 Asoperationalized by the most commonly used

measure of catastrophizing (the Pain CatastrophizingScale120), pain-related catastrophizing involves cognitiveprocesses (eg, rumination, selective focus on pain-related cognitions, and magnification of the painexperience) and cognitive content (eg, anticipation ofnegative outcomes associated with pain, and lack ofself-efficacy for pain control).103 Catastrophizing hasbeen shown to be associated with pain-related fearand decreased activity (ie, behavioral inhibi-tion46,110,115,127,137). Thus, from a BIS-BAS perspective,catastrophizing can be viewed as reflecting BIS-relatedcognitive content and processes.One of the questions that has plaguedour understand-

ing of pain-related catastrophizing might be stated asfollows: Given that catastrophizing is so clearlyassociated with negative outcomes, why do peopleengage in catastrophizing in the first place, and whywould they continue to catastrophize in response topain? One answer proposed to this question is thatcatastrophizing may play an important communicativerole in eliciting social support.121 The communal copingmodel (CCM) of catastrophizing is a theoreticalframework positing that catastrophic thoughts lead toexaggerated displays of pain behaviors (ie, grimacing,sighs, and moans), and that these pain behaviors canthen function to maximize the probability of proximityto, or to solicit assistance or empathy from, others.121

Thus, the CCM argues that catastrophizing can serve animportant social function, which leads to socialreinforcement (and more catastrophizing), via operantlearning.39 Some research in experimental and clinicalsettings has provided support for the CCM tenets thatelevated pain catastrophizing leads to an increasedpropensity to display pain behaviors,124,126 and thatexpression of pain behavior varies as a function ofsocial contextual factors.45,63,119 However, support forthe CCM is not consistent. For example, Tsui andcolleagues found that catastrophic thoughts predictedhigher levels of self-reported pain behavior but notobserved pain behavior, suggesting that shared methodvariance may have biased some of the previous researchsupporting the model.126 The CCM hypothesis that hasreceived the least research support is that pain cata-strophizers enact pain behaviors to attain interpersonalgoals.118 Severeijns et al argued that a basic cognitiveappraisal model, specifically appraisals of threat andhelplessness (ie, ‘‘BIS activation’’ using the language ofthis article), might better account for the relationshipbetween pain catastrophizing, behavioral displays ofdistress, and pain outcomes.111 Overall, the evidencesurrounding the CCM is mixed, suggesting that themodel may explain catastrophizing in some settings orfor some individuals, but not others.From a BIS-BAS perspective, the answer to why

individuals catastrophize can be stated in one word—evolution. The BIS is highly adaptive (when activated inthe appropriate context); its existence helps ensuresurvival. The BIS is particularly important in trulydangerous situations. Without a system in place thatfacilitates behavioral inhibition when needed—thatencourages us to ‘‘stop, look, and listen’’ in the


presence of danger—approach behaviors could remainunchecked, even when they could lead to negative out-comes or even death. Emotions and thoughtsfacilitated by BIS activation—fear and catastrophizing,for example—may be unpleasant when they occur, butbecause they are unpleasant, they also facilitate thebehavioral inhibition that increases our chances ofsurvival in the potentially dangerous situations94 (butsee Nettle95 for an alternative view). Thus, it makesevolutionary sense that organisms would have ahard-wired system to support behavioral inhibition andwithin this system, pain catastrophizing has adaptive aswell as (the more well-known) maladaptive qualities.The fact that behavioral inhibition can cause problems

in the context of chronic pain does not reduce itsoverwhelming survival value; survival trumps comfort.In short, a BIS-BAS model of chronic pain proposes thatbehavioral inhibition and all of the processes thatfacilitate this (including fear and catastrophizing) arenormal responses that organisms are hard-wired toactivate in response to pain. Thus, catastrophizing canalso be viewed as a normal response rather than anunusual or ‘‘exaggerated’’ response, especially in aculture in which the normative belief is that pain is anindication of physical damage (for a similar view ofcatastrophizing from a fear-avoidance model perspec-tive, see Crombez et al22).

A BIS-BAS Understanding ofPsychosocial Pain TreatmentsOur earlier formulations of the proposed model (that

did not make a distinction between BIS- and BAS-related brain states26,69) argued that 1) psychosocialpain treatments are effective because they target 1 ormore of 4 key domains (behavior, cognitions, cognitivecoping [here labeled cognitive processes], andemotions), 2) by making changes in any one of thesedomains, the other domains are influenced (ie, mutualinfluence among the hypothesized mechanisms), and 3)because of this mutual influence, changes in any 1 ofthe 4 domains can ultimately influence treatmentoutcome, including pain and pain-related disability.26,69

We had proposed that the large number of differentpsychosocial pain treatments could be understood interms of the extent to which they target and effectivelychange 1 or more of the 4 domains. Importantly, evenif different treatments appear to target different keymechanism variables (eg, behavioral activation vscognitive content), because a treatment that changesany one mechanism domain has (at least indirect)effects on all of the other factors within the system, thedifferent treatments will ultimately have similarbeneficial effects on the outcomes influenced (togreater or lesser extents) by all 4 of the mechanismvariables.The current BIS-BAS formulation makes an important

modification of these ideas in that it argues that thestrengths of the mutual effects among the domainsdiffer as a function of the type of brain state domain(BIS vs BAS) in question. Specifically for example, in

the model shown in Fig 1, BIS-related domains arehypothesized to have stronger effects on otherBIS-related domains—to in fact work in concert as a‘‘cluster’’—than on BAS-related domains, and vice versa.Our working hypothesis is that this formulation providesamore nuanced understanding of howpsychosocial paintreatments may work, and may hold promise for betterpatient treatment-matching and for enhancing the effi-cacy of pain treatment overall.As discussed previously, the BIS-BAS systems typically

function automatically (ie, on a subconscious or habitualbasis) as a response to environmental or internal cues,which have become associated with BIS or BAS via asso-ciative learning. Moreover, because the emergence ofBIS or BAS activity occurs automatically (in a trait-basedfashion), the consequences of BIS and/or BAS activationare perceived as effortless—the beliefs (alternatively,catastrophizing thoughts or confidence), emotions(alternatively, anxiety or excitement), and behavior(alternatively, withdrawal or approach behavior) emergeautomatically and without conscious effort. However, asdiscussed below, we speculate that the strength ofmutual causation among the various domains of BISand BAS can be ‘‘reprogramed’’ by psychosocial paintreatments via conscious efforts, such as a consciousevaluation of cognitive content to create newassociations and use of cognitive restructuring incognitive-behavioral therapy (CBT) or mindfulnesspractice in mindfulness-based interventions (MBIs).Because the skills taught in many pain interventions

are effortful—at least until they become habits—theymust involve a system other than BIS or BAS. Such asystem has been labeled by different theorists as the‘‘reasoning,’’ ‘‘reflective,’’ ‘‘rule-based,’’ or ‘‘system 2’’system.73,83,113,116 We propose (see next section) thatsome psychological treatments have their effects on BISand BAS, and therefore on positive outcomes, viaengagement of this separate system. However, ourmodel hypothesizes that their success in any onepatient will depend on the extent to which BIS- orBAS-related associations are ultimately influenced. Inthe proposed model, BIS and BAS activity is prominentand viewed as a final pathway that contributes to rela-tive function or dysfunction, measured using indices ofcognition, emotion, and behavior. We also proposethat some psychosocial chronic pain treatments targetprimarily BIS domains (often by reducing the chancesthat the patient will activate the BIS and inhibit activityor ‘‘step on the brakes’’ inappropriately in response topain), BAS domains (often by increasing the chancesthat the patient will activate the BAS or ‘‘press on thegas pedal’’ appropriately despite pain), or both together,and would therefore be expected to result indifferent effects on different treatment mediators andoutcomes. In the model, BIS-focused treatments arehypothesized to have a larger effect on BIS-relatedmediators (behavioral inhibition, catastrophizing,fear of movement) and outcomes (inactivity, paininterference, anxiety) than BAS-related factors, andBAS-focused treatments are hypothesized to have alarger effect on BAS-related mediators (behavioral


activation, pain-related self-efficacy, positive affect) andoutcomes (thriving, community participation) than BIS-related factors. In the paragraphs that follow, we illus-trate these points by discussing a number of the mostcommon psychosocial pain treatments from a BIS-BASperspective.

Pain Treatments That Appear to TargetBIS InhibitionCognitive therapy teaches patients to evaluate the

content of their ‘‘automatic’’ thoughts with respect tothe emotions and behaviors associated with thosethoughts.125 When the emotions and behaviors associ-ated with a specific cognition are determined to be lessthan helpful (eg, lead to sadness, fear, frustration,inactivity—ie, to facilitate BIS activation using thelanguage of the BIS-BAS model), the patient is taughtcognitive restructuring to identify, and then focus onand nurture, new thoughts that are inconsistent withthe unhelpful ones. This process is hypothesized todecrease the frequency and effect of negative thoughtsand attributions on emotions and behavioralresponses.125 In short, cognitive therapy can be viewedas a treatment that seeks to decrease pain-related BISresponses by primarily teaching skills that decrease thefrequency of BIS-related cognitive content.Of course, the identification and facilitation of adap-

tive cognitive content (ie, through the use of copingcards with statements/thoughts related to self-efficacyand hope; see Thorn125) could also increase BAS activity.Moreover, a CBT technique commonly taught to patientsis to adopt a more detached/observer relationship totheir cognitions as they evaluate those cognitions foreither encouragement (for cognitions evaluated asadaptive) or replacement (for cognitions evaluated asmaladaptive). The encouragement of adaptive thoughtsand also a more detached relationship to thoughtswould be expected to have some effect on BAS-relatedbehaviors, thoughts, and emotions, depending perhapson the focus of the specific cognitive therapy techniquesused. To the extent that the CBT treatment focuses onreducing catastrophizing, the model predicts improve-ments in BIS-related outcomes. If the CBT treatmentalso teaches patients to effectively develop and nurtureself-efficacy beliefs related to important goals, then themodel would also predict improvements in BAS-relatedoutcomes. Patients who are encouraged to adapt amore detached relationship with their cognitions wouldbe expected to report reductions in BIS- and BAS-relatedoutcomes (ie, more ‘‘acceptance’’). Thus, the effects of aCBT intervention would depend in large part on thespecific CBT techniques taught and practiced.However, the primary emphasis of cognitive therapy

has historically tended to be on the identification andelimination of negative (maladaptive) thought con-tent.125 Thus, we would hypothesize that effectivecognitive therapy, which has this focus on reducing thefrequency of maladaptive cognitions, would tend to in-fluence outcomes associated with BIS activity morethan outcomes associated with BAS activity; it would

therefore be expected to have a larger direct effect onreducing depression and behavioral inhibition than onincreasing hope, positive affect, and community integra-tion. Themodel would also predict that the patients whorespond most to cognitive therapy interventions thattarget reductions in maladaptive cognitions (eg,catastrophizing) would be patients who endorse moreBIS-related cognitive content and processes atpretreatment, rather than patients who fail to endorseBAS-related cognitive content.25

Another set of chronic pain treatments are educa-tional programs designed to explain to patients in laylanguage our current scientific understanding of chronicpain; that is, chronic pain as something that results froma combination of central nervous system and peripheralanatomic factors and thatmay act as a signal of potentialdanger, but does not directly reflect physical damage.The interventions in this category are referred to as‘‘pain neuroscience education,’’ ‘‘neuroscience educa-tion,’’ or ‘‘explain pain.’’14,20,86 These treatments usemetaphors, multimedia education, and other creativeeducational approaches to help patients understandthe important role of central sensitization and brainprocessing in the experience of chronic pain, whichthen reframes pain sensations as a reflection of thesenervous system processes rather than the result ofongoing injury. Thus, pain education helps create achange in the meaning of pain with respect to theindividual’s goal for long-term health and functionfrom 1) pain is a sign of physical damage, and thereforeneeds to be paid attention to andminimized as a priorityto 2) pain is there to protect me, and the ‘‘usual’’ chronicpain experienced does not necessarily indicate that phys-ical damage is occurring.14,92 When this new connectionbecomes automatic—which does so as patients aretaught, and engage with, the material—there is less ofa need to focus on pain (ie, BIS is not activated as muchin response to pain). This then results in a decrease inpain intensity, because of the strong influence of BISactivity on the experience of pain (Fig 1). From theperspective of Carver and Scheier’s control theorymodel,17,18 pain education can help to disconnect thelink between a higher order goal (for long-term physicalwell-being) and a ‘‘lower level’’ implication of that goal(to feel less pain). Because this treatment decreases thechances that pain sensations will be interpreted as anindication of physical harm, pain neuroscience educationis hypothesized to reduce the chances that the BIS will beactivated when the patient feels pain, and thereforehave larger beneficial effects on BIS-related outcomes(including perceived pain intensity) than BAS-relatedoutcomes.

Pain Treatments That May Target BASActivationAlthough we hypothesize that cognitive therapy

focused on reducing maladaptive cognitions and painneuroscience education interventions may have theirprimary benefits via their effect on decreasing activityin the BIS, or bymaking it less likely that painwill activate


the BIS, other treatments may have their primarybeneficial effects by increasing BAS activity. The mostobvious of these is behavioral activation, which is a com-mon component of multidisciplinary/interdisciplinarychronic pain treatment43,109 and some cognitivebehavioral therapies for pain that target activity level,specifically.35,128 Because the model hypothesizes thatchanges in any one component of the BAS (in this caseincreases in physical activity) will influence the othercomponents of the model (in this case, increases inBAS-related emotions and cognitions), the modelpredicts that simply increasing physical activity wouldhave beneficial effects on positive emotions andadaptive BAS-related beliefs. Similarly, behavioralactivation targeting other types of activity—such associal, recreational, or vocational activity—is likely toincrease BAS activity through environmental reinforce-ment, positive emotions, and adaptive BAS-relatedbeliefs. Moreover, as BAS becomes more active, someinhibition of BIS activity would be expected, whichshould result in an indirect effect in decreasing howmuch attention the individual pays to BIS-related factors,including pain and other threat-related cues.77

Motivational interviewing (MI), as it has been appliedto chronic pain, can also be viewed as an interventionthat encourages positive coping via targeted reflectivelistening that reinforces ‘‘change talk’’ (ie, BAS-relatedverbal content reflecting self-efficacy beliefs about,and the intent to engage in, adaptive coping efforts).Reinforcement of change talk reinforces the underlyingBAS-related cognitions, and subsequently an increasein BAS activity and associated outcomes occurs.67 Impor-tantly, one of the goals of MI is to encourage patients tofocus on and consider theirmost valued goals and aspira-tions90 (consistentwith Carver and Scheier’s higher-ordercontrol goals17,18), which, like ‘‘explain pain,’’ helpspatients to move away from a primary goal of merelycontrolling (or decreasing) pain.Finally, there is a growing interest in ‘‘positive

psychology’’ interventions that use strategies to targetand increase positive emotions,10,19 including the useof such treatments for chronic pain.93 Although thesetreatments do not have a clear rationale on the basis ofother theoretical models of chronic pain (which, asmentioned previously, tend to view emotional responsesas outcomes rather than causal agents), their appropri-ateness and potential efficacy are clearly hypothesizedby the BIS-BAS model presented in this article. Speci-fically, as individuals use strategies known to increasetheir experience of positive emotions, themodel predictschanges in other BAS-related variables, and to a lesserextent, BIS-related outcomes such as depression.78

Pain Treatments That May Target BIS andBAS ActivityWe have already discussed how cognitive therapy,

when it includes components that encourage patientsto take a detached stance toward their thoughts andthat encourage adaptive and optimistic cognitions(as opposed to focusing mostly on reducing the

frequency of negative cognitions) would be expected toinfluence BIS and BAS activity. Other interventions couldpotentially have such dual effects. For example, MBIs forpain, such as mindfulness-based stress reduction72 andmindfulness-based cognitive therapy28 teachmindfulnessmeditation as a core technique for coping with pain.Meditation practice is theorized to engender an‘‘observer’’ stance toward all phenomena, which is some-times referred to as defusion, reperceiving, decentering,distancing, or meta-cognitive insight.27 In a recent reviewof the literature on the mechanisms of MBIs, we notedthat the primarymechanisms specific to these approachesare emotion regulation and decoupling of sensory-discriminative and cognitive-evaluative brain networks.26

To the best of our knowledge, no research has investi-gated the associations betweenMBIs, mindfulness facets,and BIS/BAS activation in samples of individuals withchronic pain. However, one recent cross-sectional studyin an undergraduate sample found that BIS-sensitive indi-viduals report higher emotional dysregulation andunder-utilize specific mindfulness skills (of acting withawareness, nonjudgemental approach, and nonreactivityto experience).105 This same study reported that BASreward responsiveness was associated with increasedemotional dysregulation and greater tendencies toobserve and describe experience, and BAS drive was posi-tively associatedwith the ‘‘describe’’ facet ofmindfulness,and marginally negatively associated with emotionaldysregulation.105 Although the generalizability of thesefindings to clinical populations is limited, they doprovide preliminary evidence suggesting the possibilitythat different facets of mindfulness may be more or lessBIS- or BAS-sensitive, and that therefore mindfulness ap-proaches may be beneficial via their effects on BIS andBAS activity.In terms of how the facets of mindfulness (ie, cogni-

tive processes in Fig 1) may affect BIS and BAS, it ispossible that MBIs function to reduce a tendency toautomatically activate BIS or BAS in response to envi-ronmental stimuli by engendering a purposeful andeffortful ‘‘stepping back’’ from immediate environmentengagement (perhaps, for example, by purposefullyengaging in ‘‘reflecting’’ cognitive activity83); that is,to promote interaction with the environment from amore defused/decentered state. This hypothesized ef-fect of MBIs on greater flexibility—defined as an abilityto more easily and appropriately shift from BIS to BASactivation as most appropriate to the situation—maybe related to the mutual inhibitory effects of BIS andBAS activity. That is, higher levels of activity in eithersystem may make it difficult to shift into the other.MBIs, via engendering this decentered state, would beexpected to reduce activity in both systems, and there-fore would tend to have a greater effect on whicheversystem is most active. By teaching individuals to moreeasily move into ‘‘neutral’’ gear from either ‘‘forward’’(BAS) or ‘‘reverse’’ (BIS), individuals with more mindful-ness skills would be hypothesized to have an improvedability to flexibly shift between the 2 systems andrespond more appropriately to the environmentalcontext.


Acceptance and commitment therapy (ACT), which isbeing increasingly applied to chronic pain problems,88

has a focus on the function of thoughts, emotions, andbehaviors in context. Relational frame theory (RFT) isfundamental to ACT.60 Although a detailed discussionof RFT is beyond the scope of this article, a key relevantaspect of this theory is the emphasis it places on stimulusrelations (ie, relations learned without direct training)and language-based representations that are elicitedautomatically. Thus, it is a theory that focuses onassociative learning, which is hypothesized to be a keyBIS and BAS cognitive process in the current model. RFTproposes that we cannot unlearn associations that havebeen made (ie, we cannot unlearn the associationbetween verbal descriptors and the phenomenon theyrepresent). However, with new learning, we can broadenthe relational network of associations to make thenetwork more flexible and adaptive; we can createnew associations that then influence the effect of cueson thoughts, emotions, and behavior. Thus, ACT,through the development of psychological flexibility(eg, as representing primarily acceptance, defusion/observer stance, and mindfulness in this instance),broadens associative responses to different contexts,which can then result in a decreased activation of BISor BAS in certain circumstances. Further, ACTs focus onencouraging an increase in valued activities associatedwith positive meaning and roles (ie, activities thatprovide reinforcement)—similar to MI and ‘‘explainpain’’—would be expected to encourage a shift of focusfrom the ‘‘lower level’’ goal of pain reduction to ‘‘higherlevel’’ goals17—and would be hypothesized to be associ-ated with BAS activation. Thus, as with MBIs (althoughtheoretically through unique mechanisms), ACT mayalso function to optimize the balance of BIS/BAS re-sponding to flexibly adapt to changing external contextsand associated cues.Another chronic pain treatment with demonstrated

efficacy is in vivo desensitization.130,131,133 Thistreatment is based on the fear-avoidance model, and isdesigned to reduce the severity of a key emotionalresponse associated with BIS—fear; specifically, fear ofpain and movement, using a desensitizationapproach.132 But it does so, in part, using operant condi-tioning to increase behavioral activation. For this reason,we view in vivo desensitization as another treatmentthat may target BIS and also BAS activity.Finally, there has been a recent resurgence in interest

in what is perhaps the pain treatment with the longesthistory: hypnosis.66Whereas themechanisms of differenthypnosis treatments depend on the specific suggestionsoffered during treatment,62,104 all hypnotic treatmentsbegin with an ‘‘induction’’ which has been shown toincrease slow wave brain activity among individualswho are more hypnotizable, particularly in the theta(4-8 Hz) range.70 Theta oscillations are known to facili-tate new learning and memory traces,15,85 which mayexplain, at least in part, how hypnosis facilitates theease of (new) associative learning.70Moreover, perceivedeffortlessness and automaticity are central features ofhypnotic responding,84,101,107 which are also cognitive

process features of the BIS and BAS systems in ourmodel (Fig 1). As a group, these findings suggest thathypnosis could have a direct effect on creating newassociations in either the BIS or BAS (depending on thespecific suggestions offered) which then would facilitatenew automatic responses to pain or other stimuli.Hypnotic suggestions for reductions in pain and/oranxiety, that pain is not necessarily a sign of danger,and for limiting rest and inactivity would affect BISmediators and outcomes, whereas hypnotic suggestionsfor joy and optimism, increased self-efficacy, andincreased engagement in valued goals would affectBAS mediators and outcomes.

Testable Hypotheses on the Basis of aBIS-BAS Model of Chronic PainThe ideas presented in this article lead to clear testable

hypotheses that we think are unique to the BIS-BASmodel. First, to our knowledge, no other model of painpredicts stronger correlational and causal links betweenfactors within the BIS and BAS domains compared withfactors that are outside of each respective system (ie,stronger associations between measures of happiness/optimism, self-efficacy beliefs, and approach behaviorsthan between these domains and measures of sadness/anxiety, hopelessness, and withdrawal behaviors).Second, the model specifies the type(s) of maladaptive

pain-coping patterns that individuals with chronic painare likely to use, which has critical preventativepotential. For example, as discussed previously, themodel predicts that individuals with a greater traittendency for BAS activation who develop chronic painwould bemore likely to have pacing problems associatedwith ‘‘overdoing,’’ whereas those with a greater traittendency for BIS activation would be more likely tohave pacing problems associated with ‘‘underdoing.’’Again, we are not aware of any other existing modelsthat predict, a priori, who is more likely to developeach of these types of activity management problemsassociated with chronic pain.Third, the model specifies sophisticated nuanced

predictions regarding the mechanisms of the mostwidely implemented pain treatments. For example, onthe basis of our previous discussion of the targets ofcognitive therapy and ACT, we would predict that thecomponent of cognitive therapy that teaches patientsto evaluate and eliminate maladaptive thought contenthas a larger effect on measures of BIS than measures ofBAS (measured, for example, using the BIS/BAS scale).Themodel also predicts that ACTwould result in changesin BIS and BAS activity, and perhaps for this reason have alarger effect on BAS activity (and perhaps BAS-relatedoutcomes) than a cognitive therapy approach thattargets only or primarily reductions in maladaptivecognitions. In addition, the BIS-BAS model hypothesizesthat cognitive therapy’s beneficial effects on outcomeswould be mediated more by BIS-related mediators (eg,changes in catastrophizing and behavioral inhibition)than BAS-related mediators (eg, changes in positive


affect and pain acceptance), whereas the beneficialeffects of ACT may be mediated by changes in BIS- andBAS-related mediators. Research could be performed toexamine these mediational hypotheses in the contextof ongoing and future clinical trials, simply by includingmeasures of BIS and BAS activity in the assessment proto-col, and then performing appropriate analyses.12,13,102

If some of the hypotheses derived from the proposedBIS-BAS model regarding the relative effect of differenttreatments on BIS and BAS are supported, then anobvious next step would be to link the resultingknowledge regarding the relative effect of treatmentson BIS and BAS with baseline/pretreatment measures ofBIS and BAS, to determine if this model could be usedfor better patient treatment-matching.25 If, for example,an individual patient was assessed at baseline to havesignificant levels of BIS activation (ie, significantcatastrophizing, pain intensity, and deactivation), butnot a severe problem with BAS deactivation (ie, thepatient presents as being at least somewhat optimisticand with a sense of self-efficacy), then this patient mightrespond best to interventions with evidence supportingtheir ability to limit BIS. In contrast, a patient who isassessed to have very low levels of BAS, but notsignificantly high levels of BIS, may benefit more fromtreatments with demonstrated efficacy for activatingBAS. Of course, patients with very high levels of BIS andalso very low levels of BAS when pain is present maybenefit from treatments targeting both—for example,1) cognitive therapy and mindfulness to decrease BIS ac-tivity and its negative effects, and 2) ACT, MI, and/or pos-itivepsychology interventions to increaseparticipation inmeaningful activities and to facilitate feelings of hopeand positive excitement to increase BAS.

The Benefits of an Overarching Model ofChronic Pain, Such as the BIS-BAS ModelPresented in this ArticleBecause the BIS-BAS model presented in this report

introduces an additional overarching conceptual layerthat subsumes many of the current models currentlyused by scientists and clinicians to understand chronicpain and guide treatment (eg, operant theory, cognitivetheories, fear-avoidance models), a reasonable questionmight be as follows: Does the BIS-BASmodel provide anyadditional insight or utility that is not already providedby existing models? We have already addressed thisquestion in part, by discussing specific hypotheses thatemerge from the model that do not emerge from otherexisting models. However, we also believe that anoverarching model that is supported by empirical testshas the potential to broaden our understanding andability to more effectively treat individuals with chronicpain.Specifically, viewing patients only from one of the

more limited models limits the domains that areevaluated and the treatment(s) that can be offered.Clinicians operating only from an operant model wouldassess a patient’s pain behavior and the contingencies

for those behaviors,39 and perhaps only (or mostly)seek to alter the contingencies. Clinicians operatingfrom a cognitive-behavioral model might assess painbehaviors, the contingencies of those behaviors,cognitions (eg, catastrophizing thoughts,120 other painbeliefs), and coping,68 and treatment would be (primar-ily) limited to discouraging the use of maladaptivecognitions and coping responses and to teaching andencouraging the use of more effective pain-copingstrategies. However, clinicians operating from a BIS-BASmodel would seek to assess each component of themodel (eg, environmental responses, brain states, aswell as BIS- and BAS-related cognitions, emotions, andbehavior). Depending on the outcome of the assessment,a BIS-BAS clinician could then target the appropriateintervention or technique (including, but not limitedto, operant conditioning, training in mindfulness,relaxation, or self-hypnosis, cognitive restructuring,behavioral activation, etc) to activate appropriateresponses, limit inappropriate responses, and/orenhance skills or strengths thatmay already be present.25

Thus, the BIS-BAS overarching model provides a theoret-ically driven approach for tailoring interventions topatient characteristics; it could match patients with themost appropriate treatment components and focustreatment efforts on the strategies most likely to benefitindividuals. This could also make treatment moreefficient and less costly, by focusing more on what ismost needed by each individual patient.

Limitations of a BIS-BAS Model of ChronicPainAny model that seeks to explain the complexity of

chronic pain by focusing on a subset of just a fewdomains and their interactions has limitations. Fromour perspective, the most important limitations ofthe proposed BIS-BAS model are that 1) it is incom-plete—there are more than just 2 neurophysiologicalsystems that explain behavior; 2) it does not (yet)explain the specific processes involved in BIS and BASactivation; 3) it assumes that the BIS and BAS have atleast some state qualities and are modifiable, however,this has not yet been proven; and 4) there are limitedmeasures of BIS and BAS activity that can be used totest the model in populations of individuals withchronic pain.

The Model Is IncompleteGray’s BIS-BAS model and other 2-factor models of

behavioral and emotional responses do not explainall possible human responses. For example, whereasmeasures of BIS and BAS are associated with 2 of thebig 5 personality traits in ways consistent with 2-factor models (ie, with neuroticism and extraversion,respectively31,48,53,114), they tend to be only weaklyassociated with the other 3 personality traits(openness, conscientiousness, and agreeableness);there is more that underlies human behavior thanwhat is accounted for by the BIS and BAS. That said,


it is not clear or obvious how the personality domainsof openness, conscientiousness, and agreeablenesswould affect or explain the efficacy of paintreatments, especially to the same extent of BIS(neuroticism) and BAS (extraversion). Also, we areaware of no evidence supporting an important roleof these other personality domains (openness,conscientiousness, and agreeableness) in pain. Still, itis unlikely that measures of BIS and BAS activity willbe found to mediate all of the beneficial effects ofcurrent and future pain treatments, or that onlytreatments that affect BIS and BAS will ultimately befound to be helpful.One of the most obvious systems missing from our

proposed BIS-BAS model is one that has been includedin Gray’s model from the 1980s; the fight-flight system(1980s) or what he later labeled the fight-flight-freezesystem (FFFS54). This system is not included in most other2-factormodelsbecause thebehaviors andemotions theyare thought to facilitate (fighting, freezing, runningaway, rage, panic) are not commonly experienced on adaily basis by most people; that is, the FFFS does notplay a significant role in most people’s day-to-day func-tioning. However, there are clearly individuals withchronic pain for whom the FFFS may play a more promi-nent role, for example, individuals with chronic painand post-traumatic stress disorder.112 Like most other 2-factor theorists, we elected not to incorporate the FFFSinto our BIS-BAS model at this time in part to keep themodel more focused, and also because the FFFS doesnot play a prominent role in responses to chronic painformost individuals.However, if future research indicatesthat the BIS-BAS model that we propose in this articleproves to beuseful,we can envisionmodifying it to incor-porate the FFFS (or other systems that are subsequentlyidentified as playing an important role in response tochronic pain) in the future.Another system missing from our proposed BIS-BAS

model has been mentioned in this article, and hasbeen referred to as the ‘‘reflective’’ system, amongother labels.73,83,113,116 Unlike BIS-BAS, which respondsquickly, automatically, and without perceivedeffort, the reflective system is slow, more controlled,and requires effort to maintain. This latter featuremakes the reflective responding difficult to sustain. Asa result, it may have limited effect on our day-to-dayexperience or behavior. Reflective responses havebeen described as being ‘‘.like cavalry charges in abattle—they are strictly limited in number, they requirefresh horses, and must only be made at decisivemoments.’’quoted in 83 p 14 Reflection is thought to becomeengaged when the BIS-BAS subsystems are stymied, andit becomes clear that a more thoughtful (slow, delib-erate, logical) response is required.73 However, the BIS-BAS systems are rarely stymied, because they are fairlyefficient. The model hypothesizes that it is via theengagement of the reflective system that traditionalcognitive therapy operates—to slow down and logicallyexamine the automatic thoughts generated by BISand BAS and then via rational consideration identifyalternative more useful thoughts to be considered and

nurtured. But in general, unless the reflective system isspecifically called upon, ‘‘.like the refrigerator light,[it] is always on when we check it; but like therefrigerator light, it is probably off more often thanon.’’83 p 14

The model, as presented in this article, does notdescribe how BIS and BAS activity interacts with otherneurophysiological processes and systems likely associ-ated with pain. These include, for example, thehypothalamic-pituitary-adrenal axis and autonomic ner-vous system responses,61,136 hormone abnormalities,123

neurotransmitters,37,79 and the immune andneuroendocrine systems.30,89 If future research providesadditional support for the BIS/BAS model presented inthis article, empirical examinations of how these othersystems and processes interact with (or may even beimportant aspects of) BIS and BAS would be useful.Finally, the model as presented is a static ‘‘snapshot’’

model of chronic pain. However, people live in a realworld that constantly changes; potential punishmentand opportunities for reward appear and then fadeinto the background. As mentioned earlier in this article,the BIS-BAS system is dynamic, and constantly influx. Goal-related BIS and BAS activation (to avoidpunishment and obtain rewards, specifically) increasesand decreases as the possibility of punishment fadesand as rewards are obtained (ie, as goals are met). Unlikethe model presented in this report, other models focusmore on how motivational processes change overtime.18,75 Future iterations of the BIS-BAS model—ifenough of the components of the model are supportedto warrant its continued development—should seek totake into account these dynamic processes andmechanisms, so as to identify critical points forinfluencing those processes.

The Model Does Not (Yet) Explain theProcesses Involved in BIS and BASActivationA second limitation of the existing 2-factor models,

including the model presented in this report, is thatthey focus mostly on the effects of BIS and BAS onbehavior, cognitions, and emotions, and do not focuson the factors that contribute to BIS and BAS activation.Although Gray’s 2-factor model proposes that the BISand BAS are activated in the presence of cues indicatingthe possibility of punishment (BIS) or reward (BAS) onthe basis of previous learning, the model presented inthis report and other models are short on details thatdescribe the specific processes involved in this activation.The specific role(s) thatattributions, behaviors, biologicalprocesses, cultural context, and ongoing (baseline) emo-tions play in this process are not yet specified in thesemodels or by the initial BIS-BAS model of chronic painpresented in this report. Such specificationwould be use-ful, although again we think that it would make moresense tofirst determine if thehypotheses that are derivedfrom the model as presented are supported by researchfindings before modifying it to better understand thefactors that influence BIS and BAS.


The Model Does Not Specify the Extentto Which Trait BIS and BAS Activity AreModifiableThere is evidence that BIS and BAS have trait proper-

ties, but there is little information regarding the overallmodifiability of BIS and BAS activation. Thus, we do notyet know the extent to which someone’s predispositionto respond to environmental cues with BIS activation(ie, someone with a dysthymic disorder, such as ‘‘Eeyore’’in the Winnie-the-Pooh stories91) or BAS activation (ie,someone who appears to be fearless or to act with littleinhibition, such as ‘‘Tigger’’ in the Winnie-the-Poohstories91) can be changed with treatment, or moreimportantly, how long any changes that are made last.Perhaps baseline or trait BIS or BAS activity cannot bealtered permanently, so that all we can do is teach skillsthat (when mastered and used frequently) inhibit BISactivation or BAS activation (eg, mindfulness) to restorea more adaptive BIS-BAS balance or an ability to moreflexibly shift BIS and BAS activation most appropriatelyin context, without having any influence on the baselinepredisposition.

Limitations in the Availability ofMeasures of BIS and BAS ActivityAccurate assessment of BIS and BAS activity is essen-

tial for the treatment-matching proposed by the modelpresented in this report, as well as for the furthertesting and development of the model. Although theBIS/BAS scale18 has been used extensively in the person-ality and psychopathology domains,3,7,9,31,48,53,55,56,114

the measure was not specifically designed to assess BISor BAS activation with respect to chronic painconditions. An important next step in the evaluation

and development of the model presented would beto develop such a measure.

Summary and ConclusionsA great deal of support exists for the conclusion that

2 distinct neurophysiological systems underlie approachand avoidance behaviors and their associated emotionsand cognitions. In this article we propose a 2-factormodel of chronic pain on the basis of these 2 systems.The proposed BIS-BAS model appears to have a greatdeal of explanatory power for understanding the fac-tors that underlie pain-related cognitions and cognitiveprocesses (eg, catastrophizing), emotions (eg, fear ofmovement), and behavior (eg, pacing problems anddisability) and the psychological treatments thataddress these factors. A number of specific testable hy-potheses emerge from the model, and the model alsosuggests several strategies for better patienttreatment-matching and for enhancing the benefits ofpsychological treatments. Research to test the hypothe-ses that emerge from the model and to evaluate therelative efficacy of the treatments suggested by themodel are warranted as a way to better understandthe mechanisms that underlie psychological pain treat-ments and to better match patients to the treatmentsthat may be most effective for them. Ultimately,research in this area may improve our ability to help pa-tients more successfully manage pain and its effect ontheir lives.

AcknowledgmentsThe authors thank Lisa C. Murphy and L. Charles Ward

for their helpful review and comments on earlier versionsof this report.

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