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Pain catastrophising: How can we best deal with it?



The 2024 Global Year will examine what is known about sex and gender differences in pain perception and modulation and address sex-and gender-related disparities in both the research and treatment of pain.

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Jack: “Ouch, my head hurts!”

Jill: “Don’t freak out, Jack.”

Jack: “Why not? It hurts!”

Jill: “Yeah but freaking out will only make it worse.”

Jack: “How do you know? It might make it better.”

Jill: “I’ve read the science, Jack. I know. Just take a few breaths. Come on, let’s walk over to that tap and fill up your bucket.”

Jack: “OK… [Jack walks, breathes…] You know what, Jill? It kind of feels a bit better. I told you freaking out worked. It made you give me those groovy tips.”

What does it mean to freak out about your pain and what can you do about it? In research jargon, we’re talking about pain catastrophising of course, what Mick Sullivan describes as “an exaggerated negative mental set brought to bear during actual or anticipated painful experience”.[1] The most widely used tool for measuring it, the Pain Catastrophizing Scale,[2] suggests three core components: a tendency to magnify the threat value of pain, to get stuck ruminating about it, and to feel helpless about your ability to cope with it.

Pain catastrophizing (PC) is one of the most widely studied psychological constructs in pain science and perhaps the strongest psychological predictor of poor pain outcomes [3]. The more you freak out, the worse things get.

For example, elevated PC is associated with greater disability,[4] pain intensity,[1] depression,[5] anxiety,[6] work absenteeism,[7] opioid misuse,[8] and health-care utilisation.[9] As a lynchpin of the fear-avoidance model, [10-12] PC predicts the transition to chronicity [13] and mediates outcomes for a range of interventions. [14-19]  PC is also linked to biological processes that could modulate nociception, such as dysregulation of the hypothalamic-pituitary axis, [20,21] reduced descending inhibitory control through endogenous opioid pathways;[22] and pain-facilitating changes in functional connectivity of the brain’s default mode network.[23]

Sounds bad. So, if I score highly (e.g. >24 out of 52 [24]) on the PCS after a tumble down the hill, what should I do? This was the question we asked recently, culminating in a systematic review and meta-analysis of interventions for PC in adults with chronic non-cancer pain. [25] We wanted to compare interventions from quality, published RCTs to see if a gold standard treatment could be found. We had noticed that a range of different therapies seemed to work and were trying to make sense of evidence that CBT, exercise, and multimodal treatment performed about the same (but only modestly). [26]

We ended up comparing 79 studies with 9,914 people undertaking 17 different types of treatment, such as acceptance and commitment therapy (ACT), acupuncture, CBT, education, exercise, graded exposure, hypnosis, mindfulness, multimodal treatment, pharmacotherapy and yoga. We considered trials that either targeted PC directly or included it as a secondary outcome, and we performed sub-group analyses on the targeted interventions to see if targeting made a difference. By far the most common intervention was CBT and the most widely studied form of pain was spinal pain, particularly low back pain.

Crunching together the effect sizes of these studies in our meta-analyses showed that 9 different interventions had some kind of efficacy (statistical significance) compared with either usual care or an active control, although the quality of this evidence was often low according to GRADE criteria. [27] The biggest problem was heterogeneity, or the fact that effect sizes varied a lot between different studies of the same intervention. This may have been related to the significant variation in treatment content, dose, setting and clinical cohort within each intervention type. Generally, the quality of the studies was pretty good, with about 60% judged at low risk of bias using a modified Cochrane bias tool that considered blinding of participants and assessors but not therapists. [28]

Three interventions stood out when we focused on the moderate-high quality evidence: CBT, multimodal treatment, and ACT. Multimodal treatments that combined CBT with exercise seemed to have the strongest effects (e.g. SMD = -1.0 compared to active control; 10 studies, N = 1,258). However, there was a lot of variation within this estimate. It was inflated by some very large effects from a single research group, so we need more research to confirm this. Nevertheless, it seems plausible that multimodal treatment could perform well given that the treatment components could have additive effects. We speculated, for example, that the thought challenging exercises used in CBT might be boosted by the experience of exercising without catastrophic outcomes (i.e. both components lead to reduced threat magnification).

Sadly, most interventions produced only moderate reductions in PC (e.g. SMD = .3–.8), which translates to about 3-7 points on the 52-item PCS. On a clinical level, our estimate that the minimum clinically important difference on the PCS is about 5 points suggests that only multimodal treatment was effective (considering just the moderate-high quality evidence).

Interestingly, things changed a little when we considered the moderating effect of things like: baseline catastrophising, whether PC was targeted as a primary outcome, risk of bias rating, treatment length, and pain condition, amongst others. Using meta-regression, we found that the most common moderators were baseline PC and whether PC was a primary outcome. In fact, when we only looked at ‘targeted’ studies (i.e. those targeting PC as a primary outcome and enrolling cohorts with clinically significant catastrophising), the effects were larger and the stand-out treatment was CBT. For example, the effect of CBT versus active control increased from SMD = -0.47 to SMD = -0.84. CBT was also the only effective treatment in the active control group analyses. However, there were only 8 ‘targeted’ studies overall, so the superiority of CBT here probably just reflects the lack of targeted research on PC for the other interventions.

If this is all making your head hurt, then: a) me too; b) try not to catastrophise; and c) here are some simple take home messages. PC is a modifiable characteristic. There’s no real gold standard yet because we need more targeted research, but CBT, multimodal treatment (CBT + exercise) and ACT look pretty good so choose one of them for now if you’re a clinician. In the future, to get more bang for our bucks, it might be best to try and match specific catastrophising phenotypes to different treatment components. An over-simplified example might be that someone really high on the rumination subscale of the PCS might do better with ACT while someone high on the magnification subscale is more suited to a CBT approach that targets specific threat cognitions. To get to the bottom of this, as always, we need more research – more people sitting around ruminating about pain rumination.

About Rob Schütze

Rob is a clinical psychologist in private practice (Wisdom Health, Perth Australia) whose main clinical interest is working with people experiencing persistent pain. He has just finished a PhD at Curtin University looking at the role of metacognition in pain-related rumination. In 2018, he will be working on the RESTORE clinical trial investigating individualised movement rehabilitation for chronic, disabling low back pain (Curtin University & Macquarie University). In his spare time, Rob enjoys tumbling down hills, preferably on a mountain bike or snowboard.


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