The impact of pain on motivation:  Should I stay or should I go?

Contemporary biopsychosocial models of chronic pain argue that the experience of pain emerges, and is influenced by, an interaction and integration of biological, psychosocial, and social factors.[1]  However, among scientists who study biopsychosocial models, the “bio” part of the model is often underdeveloped.  A greater understanding of how biological factors interact with psychological and social factors in the experience of chronic pain may improve our ability to integrate biological with psychosocial interventions and contribute to the development of more effective treatments.

Two biological brain systems that could potentially play a role in how people respond to chronic pain are the so-called behavioural inhibition and behavioural activation systems (BIS and BAS, respectively).[2, 3]  These systems are hypothesised to play key roles in people’s decisions regarding whether to: (1) actively pursue their goals and experience reinforcement or (2) become inactive (“stop, look, and listen”) and scan the environment for danger.  The idea here is that the “approach” (or BAS) system facilitates a set of pre-wired behaviours (e.g., more activity, exploration, and “approach” behaviours), emotions (e.g., joy, excitement, hope), and thoughts (e.g., positive thoughts regarding self-efficacy).  On the other hand, the “withdrawal” (or BIS) system is hypothesised to facilitate a different set of behaviours (e.g., inactivity), emotions (e.g., fear), and thoughts (e.g., negative thoughts about real or imagined danger).  Critically, the two systems are hypothesised to be independent, much like the acceleration and braking systems of a car.

We recently hypothesised that these two systems may be influenced by – and also influence – the experience of pain and how people respond to pain.[4]  Specifically, we hypothesised that pain usually activates the BIS system and that when the BIS system is activated, a person is more likely to interpret sensations as pain; that is, pain is viewed as both a cause and result of BIS activation.  We also hypothesised that when the BAS system is activated, a person is less likely to experience pain or be negatively influenced by pain.  However, because pain is more closely linked to the BIS system (as a signal of danger), we hypothesised that the associations between BIS and pain would be stronger than those between BAS and pain.

To test these hypotheses, we administered a commonly used measure of BIS and BAS activity (the BIS/BAS scale[5]) to 563 college students, along with (1) measures of their average pain intensity at 10 body sites in the past week and (2) the frequency with which they experience mild, moderate, and severe headaches.  We found that, as predicted, the measure of BIS activity was significantly positively related to both pain intensity and the frequency of mild, moderate, and severe headaches; that is, more BIS activity was associated with more pain.  The measure of BAS activity was associated significantly (and negatively) only with the frequency of severe headaches, and this association was weaker than that found for BIS activity.  In short, the findings provided support for a BIS-BAS model of pain.

To our knowledge, this study was the first time that the associations between measures of BIS or BAS activity and pain have been examined and reported.  Therefore, more research in other samples of individuals with pain is needed to determine whether the findings are reliable.  However, if the findings are found to be reliable, a BIS-BAS model of pain may prove to be very useful for understanding and treating chronic pain problems.

For example, the model suggests that treatments for chronic pain might be more effective if they target both the BIS and BAS systems, rather than just one or the other.  Many of the most commonly used psychosocial pain treatments can be viewed from a BIS-BAS perspective as targeting a reduction in BIS activation (e.g., to reduce or eliminate BIS-related catastrophising cognitions[6] or to teach patients about the neurophysiology of pain so that pain is no longer seen as a signal of physical damage which produces fear and withdrawal or inactivity[7]).  “Positive psychology” interventions, on the other hand, can be viewed as targeting an increase in BAS activity by encouraging patients to focus on their most valued goals (instead of pain) and to experience positive emotions (e.g., [8, 9]).  Treatment packages that target both BIS and BAS would be hypothesised to be more effective, on average, than those that target just one or the other.  Similarly, a BIS-BAS view would argue that tailoring treatment more appropriately – for example, by using cognitive therapy to reduce negative cognitions among patients who show too much BIS activation and using positive psychology interventions to increase positive emotions among patients who show low levels of BAS activation – would result in better outcomes than just giving every patient the same treatment.

However, before we systematically change how we evaluate patients for and provide chronic pain treatment based on a BIS-BAS model, more research is needed to better understand the model’s strengths and weaknesses.  We need to determine, for example, if measures of BIS and BAS associated with pain and pain severity across different populations of individuals with chronic pain.  It would also be useful to determine if treatments that are hypothesised to produce their benefits because they reduce BIS activity, increase BAS activity, or both, actually have the hypothesised effects on measures of BIS and BAS.  We also need to find out whether the effects of the treatments on measures of BIS and BAS mediate (or explain) the benefits of those treatments, as hypothesised.  If the model continues to be supported, it may prove to be a useful way to understand the biological systems that underlie pain and response to pain treatment.  This could then lead to the development of more effective pain treatments, which is arguably the most important goal of pain research.

About Mark Jensen

Mark P JensenMark P. Jensen, is a Professor and Vice Chair for Research in the Department of Rehabilitation Medicine, University of Washington School of Medicine. Dr. Jensen’s research program focuses on the development and evaluation of psychosocial interventions for pain management.  He has been awarded a number of grants from the National Institutes of Health and other funding sources for this work, and is the author or co-author of over 400 articles and chapters.  He has received a number of awards from the American Psychological Association (2003 APA Division 30 Award for Best Clinical Paper and 2012 Award for Distinguished Contributions to Scientific Hypnosis), the Society for Clinical and Experimental Hypnosis (Roy M. Dorcus Award for Best Clinical Paper, 2004), and the American Society of Clinical Hypnosis (Clark Hull Award for Scientific Excellence in Writing on Experimental Hypnosis, 2009) for his scientific contributions.  He is the author of Hypnosis for chronic pain management, which won the 2011 Society for Clinical and Experimental Hypnosis Arthur Shapiro Award for Best Book on Hypnosis.  He is also the current Editor-in-Chief of the Journal of Pain.

References

  1. Novy, D.M., et al., Perspectives of chronic pain: an evaluative comparison of restrictive and comprehensive models. Psychological Bulletin, 1995. 118(238-247).
  2. Gray, J.A., Brain systems that mediate both emotion and cognition. Cognition and Emotion, 1990. 4(3): p. 269-288.
  3. Fowles, D.C., The three arousal model: implications of gray’s two-factor learning theory for heart rate, electrodermal activity, and psychopathy. Psychophysiology, 1980. 17(2): p. 87-104.
  4. Jensen, M.P., G. Tan, and S.M. Chua, Pain Intensity, Headache Frequency, and the Behavioral Activation and Inhibition Systems. Clin J Pain, 2015. 31(12): p. 1068-74.
  5. Carver, C.S. and T.L. White, Behavioral inhibition, behavioral activation, and affective responses to impending reward and punishment: The BIS/BAS Scales. Journal of Personality and Social Psychology, 1994. 67: p. 319-333.
  6. Thorn, B.E., Cognitive therapy for chronic pain : a step-by-step guide. 2004, New York: Guilford Press. xxiv, 278 p.
  7. Moseley, G.L. and D.S. Butler, Fifteen Years of Explaining Pain: The Past, Present, and Future. J Pain, 2015. 16(9): p. 807-13.
  8. Bolier, L., et al., Positive psychology interventions: a meta-analysis of randomized controlled studies. BMC Public Health, 2013. 13: p. 119.
  9. Muller, R., et al., Effects of a Tailored Positive Psychology Intervention on Well-Being and Pain in Individuals With Chronic Pain and a Physical Disability: A Feasibility Trial. Clin J Pain, 2016. 32(1): p. 32-44.

Comments

  1. Sewika Sulpe says

    Hello mark. I am a bachelor in Physiotherapy student from Nepal.Its so great to read up your articles and this one is much interesting too. Sir i really loved this BIS-BAS system and i would love to know it more.
    Sir. Can i get some links to explore the topic? It would be really helpful to me.
    Thank you sir.

    Regards!

  2. John Quintner says

    Mark, thank you for posting your thoughtful article and directing me to your co-authored 2015 paper.

    What caught my attention was your reification of the experience of pain. In other words, a sensory and emotional experience is being portrayed as a concrete entity that seems to possess agentive properties:

    “Specifically, we hypothesised that pain usually activates the BIS system and that when the BIS system is activated, a person is more likely to interpret sensations as pain; that is, pain is viewed as both a cause and result of BIS activation.”

    In your paper, drawing upon the work of Vlaeyen and colleagues, I found the following example of reification: “These considerations suggest that pain, especially perhaps moderate to severe pain, would engage BIS, and that BIS activity might then underlie both pain-related fear reactions and subsequent pain-related behavioral interruption and inhibition (eg, rest and inactivity).

    Have I misunderstood your position?

  3. Basically, anxiety predicts pain. I feel like we should welcome the simplicity of this and not attempt to create new models if they are not needed.

    Whether to treat the anxiety, encourage goal-seeking or both? This has been researched already. Here’s what was found:

    – The therapist must never attempt to counter negative emotions or thoughts. He must adopt a ‘pro-symptom position’.
    – He should aim to provide Presence in order to uncover layers of emotions in the client. There will almost always be layers.
    – When the core negative emotion is reached, a degree of release will occur, so long as the therapist remains Present. If the therapist doesn’t know how to be Present, then emotions remain blocked.

    ONLY ONCE this stage has been achieved should reframing be attempted (if at all). Release and/or reframing allows the client to gradually move back into goal-seeking mode. We need not encourage goal-seeking because it’s a natural and deeply ingrained drive. To encourage goal-seeking is therefore poor practice. All we need to do is assist the client to remove the blocks to natural growth. The client will subsequently be capable of realizing his own inner drives for growth.

    John Quintner Reply:

    EG, in my opinion you are spouting psychological jargon that falls under the category of “psychobabble”. But I do concede that others may find your ‘mentalist’ approach to be useful.

    A ‘mentalist’ holds that we can tell a coherent and genuine explanatory mental story about mental phenomena.

    Reference: Gillett GR. The neurophilosophy of pain. Philosophy 1991; 66: 191-206.

    EG Reply:

    The whole idea of BIM is to present ‘research of the brain and mind in chronic pain’. That’s the area of interest – mind/brain/pain. If talk about psychology makes you feel uneasy, I’m sure there are plenty of forums where a rigid adherence to old fashioned biomedical models is encouraged.

    The question I asked you earlier remains unanswered. How did you used to treat patients in pain? Did they get good outcomes? Did you cure anyone? Because the thing is this – patients aren’t interested in verbose, intellectual posturing between colleagues, and neither am I. Not in the least. I’m intersted in uncovering the most rapid and complete pain relief possible. What’s your interest?

    Mark’s research found anxiety predicts pain – ok good. To promote a new model (BIS-BAS) is to add a layer of complexity to an already overly complex field. Also, some of the areas highlighted for future research have already been extensively researched to the point of completion. It’s not acceptable to treat research as a personal indulgence whilst people are waiting for pain relief. I’m not suggesting Mark is doing this, but I have seen so many pain researchers who do exactly this. It’s almost like they use the job to explore their own vocabulary and promote their intellect.

    It’s not about intellectual indulgence, ‘journal-status’ and PhDs. It’s about clinical outcomes for actual people.

    John Quintner Reply:

    Please be patient. I have asked the Chief Editor to publish material that may well answer your questions, at least in part. As I have pointed out, the rules of Body in Mind are specific – “Promotion of your particular therapy in the comments section is not appropriate here …” By the way, has your own research ever been published?