Cognitive behavioural therapy reduces central sensitization
Pain is not a simple sensory experience. Negative thoughts about the meaning of pain or unpleasant emotions like fear and depression can, in some cases, cause more suffering than the actual sensation. Psychological treatments like cognitive behavioural therapy (CBT) target thoughts and emotions associated with pain and have shown effectiveness in halting the cycle of depression and disability that frequently accompanies chronic pain.[1]
Despite the effectiveness of these treatments, they do not work for everyone. Improving the effectiveness of psychological therapies requires a better understanding of how they work. One key question is whether these treatments only change cognitive and emotional responses or whether they actually change the sensory experience of pain. In other words, can changing our pain-related thoughts actually change our sensitivity to peripheral input that causes pain?
Brain stem regions like the periaqueductal gray (PAG) and rostral ventromedial medulla (RVM) can send descending signals to the spinal cord to either increase or decrease the level of sensitivity to incoming nociceptive signals (the peripheral input that usually initiates pain). These regions are connected to cortical and subcortical regions involved in cognition and emotion, allowing pain sensitivity to be modulated by thoughts and feelings.[2] Consistent with this possibility, numerous neuroimaging studies have demonstrated an association between cognitive modulation of pain and coactivation and/or functional connectivity of cortical regions and descending modulatory circuitry.[3-6] What has not been established is whether this circuitry can be trained: can teaching people to alter their cognitive and emotional responses to pain actually change their sensitivity to sensory input?
To investigate this, we designed an experimental model of CBT.[7] Healthy, pain free participants received 45 short bursts of painful heat to their non-dominant forearm in each of eight sessions. We measured the intensity and unpleasantness of pain as well as secondary hyperalgesia, which is increased pain sensitivity of the undamaged area around a wound. Secondary hyperalgesia is the product of sensitization of the central nervous system. In addition to the spinal cord, this sensitization has been linked to descending modulatory regions like RVM,[8] suggesting the possibility that this sensitization could be subject to top down modulation based on thoughts and feelings. We therefore hypothesized that CBT could reduce secondary hyperalgesia.
Prior to each session, half of the subjects were given a short (five minute) session of CBT based on a published treatment manual.[9] They were encouraged to reduce negative thoughts about the thermal pain and to focus on positive aspects of the training (e.g. learning pain coping skills to be used in the future). The rest of the subjects were given training that did not focus on pain (focusing instead on improving interpersonal relationships).
As we expected, CBT reduced self-reported pain unpleasantness but not intensity, suggesting that the training altered the emotional response to pain. More intriguingly, the CBT group showed a 38% reduction in the size of the secondary hyperalgesic area while the control group’s secondary hyperalgesia was not reduced.
These results demonstrate that psychological training can reduce central facilitation of pain. This finding is clinically important because central sensitization has been demonstrated in many chronic pain conditions.[10, 11] These results suggest that reduction in such sensitization might be one mechanism whereby CBT imparts its beneficial effects. Future research might focus on how individual differences in the degree to which these responses can be trained might underlie differences in how individuals respond to CBT and other psychological treatments.
About the authors
Karen Davis
Karen D. Davis, PhD is a Professor in the Department of Surgery and Institute of Medical Science at the University of Toronto, and heads the Division of Brain, Imaging and Behaviour – Systems Neuroscience at the Toronto Western Research Institute.
Tim Salomons
Tim V. Salomons, PhD is a Marie Curie International Incoming Fellow and Assistant Professor in the School of Psychology and Clinical Language Science at the University of Reading, UK. He is interested in the cognitive and biological mechanisms that make pain salient and how individual differences in these mechanisms might underlie differences in coping and treatment response.
References
[1] Williams, A. C. de C., Eccleston, C. & Morley, S. Psychological therapies for the management of chronic pain (excluding headache) in adults. Cochrane Database Syst. Rev. Online 11, CD007407 (2012).
[2] Fields, H. L., Basbaum, B. & Heinricher, M. M. in Textbook of Pain 125–142 (Elsevier, 2006).
[3] Bingel U, Lorenz J, Schoell E, Weiller C, & Büchel C (2006). Mechanisms of placebo analgesia: rACC recruitment of a subcortical antinociceptive network. Pain, 120 (1-2), 8-15 PMID: 16364549
[4] Eippert F, Bingel U, Schoell ED, Yacubian J, Klinger R, Lorenz J, & Büchel C (2009). Activation of the opioidergic descending pain control system underlies placebo analgesia. Neuron, 63 (4), 533-43 PMID: 19709634
[5] Salomons TV, Johnstone T, Backonja MM, Shackman AJ, & Davidson RJ (2007). Individual differences in the effects of perceived controllability on pain perception: critical role of the prefrontal cortex. J Cogn Neurosci., 19 (6), 993-1003 PMID: 17536969
[6] Kucyi A, Salomons TV, & Davis KD (2013). Mind wandering away from pain dynamically engages antinociceptive and default mode brain networks. Proc. Natl. Acad. Sci U.S.A., 110 (46), 18692-7 PMID: 24167282
[7] Salomons TV, Moayedi M, Erpelding N, & Davis KD (2014). A brief cognitive-behavioural intervention for pain reduces secondary hyperalgesia. Pain, 155 (8), 1446-52 PMID: 24569149
[8] Urban MO, & Gebhart GF (1999). Supraspinal contributions to hyperalgesia. Proc. Natl. Acad. Sci. U.S.A., 96 (14), 7687-92 PMID: 10393881
[9] Thorn, B. Cognitive Therapy for Chronic Pain: A Step-by-Step Guide. (The Guilford Press, 2004).
[10] Arendt-Nielsen L, & Yarnitsky D (2009). Experimental and clinical applications of quantitative sensory testing applied to skin, muscles and viscera. J Pain, 10 (6), 556-72 PMID: 19380256
[11] Edwards RR (2005). Individual differences in endogenous pain modulation as a risk factor for chronic pain. Neurology, 65 (3), 437-43 PMID: 16087910