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Review
. 2021 Mar 23:12:630422.
doi: 10.3389/fpsyg.2021.630422. eCollection 2021.

What Does CATS Have to Do With Cancer? The Cognitive Activation Theory of Stress (CATS) Forms the SURGE Model of Chronic Post-surgical Pain in Women With Breast Cancer

Affiliations
Review

What Does CATS Have to Do With Cancer? The Cognitive Activation Theory of Stress (CATS) Forms the SURGE Model of Chronic Post-surgical Pain in Women With Breast Cancer

Alice Munk et al. Front Psychol. .

Abstract

Chronic post-surgical pain (CPSP) represents a highly prevalent and significant clinical problem. Both major and minor surgeries entail risks of developing CPSP, and cancer-related surgery is no exception. As an example, more than 40% of women undergoing breast cancer surgery struggle with CPSP years after surgery. While we do not fully understand the pathophysiology of CPSP, we know it is multifaceted with biological, social, and psychological factors contributing. The aim of this review is to advocate for the role of response outcome expectancies in the development of CPSP following breast cancer surgery. We propose the Cognitive Activation Theory of Stress (CATS) as an applicable theoretical framework detailing the potential role of cortisol regulation, inflammation, and inflammatory-induced sickness behavior in CPSP. Drawing on learning theory and activation theory, CATS offers psychobiological explanations for the relationship between stress and health, where acquired expectancies are crucial in determining the stress response and health outcomes. Based on existing knowledge about risk factors for CPSP, and in line with the CATS position, we propose the SURGEry outcome expectancy (SURGE) model of CPSP. According to SURGE, expectancies impact stress physiology, inflammation, and fear-based learning influencing the development and persistence of CPSP. SURGE further proposes that generalized response outcome expectancies drive adaptive or maladaptive stress responses in the time around surgery, where coping dampens the stress response, while helplessness and hopelessness sustains it. A sustained stress response may contribute to central sensitization, alterations in functional brain networks and excessive fear-based learning. This sets the stage for a prolonged state of inflammatory-induced sickness behavior - potentially driving and maintaining CPSP. Finally, as psychological factors are modifiable, robust and potent predictors of CPSP, we suggest hypnosis as an effective intervention strategy targeting response outcome expectancies. We here argue that presurgical clinical hypnosis has the potential of preventing CPSP in women with breast cancer.

Keywords: breast cancer; chronic postsurgical pain; cognitive activation theory of stress; expectancies; hypnosis; predictive coding; sickness behavior; stress.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The cognitive activation theory of stress (CATS; Ursin and Eriksen, 2010). The stress stimulus (load) is registered. Stimulus- and response- outcome expectancies influence whether the load is appraised as stressful. If so, a general physiological stress response is activated. Feedback from the physiological stress response is being fed back to the brain. A short activation of the stress response is healthy and adaptive, while a sustained stress response may lead to illness or disease. Reprinted from Ursin and Eriksen (2010), Copyright (2021) with permission from Elsevier.
Figure 2
Figure 2
The SURGE Model of chronic post-surgical pain in women with breast cancer: surgery activates the central nervous system and creates acute pain. In line with CATS- and predictive-coding framework principles, the pain is appraised based on previous experiences in form of response outcome expectancies. An expectancy of being able to handle the pain with a positive outcome (coping) dampens or eliminates the physiological stress response. An expectancy of not being able to control or influence the pain (helplessness) or only making the pain worse (hopelessness) sustain the activation of the stress response. The sustained activation creates a vicious cycle of chronic stress, chronic inflammation, and chronic pain mediated by pathophysiological mechanisms such as central sensitization, cortisol dysfunction, impairment of corticolimbic connectivity, and inflammatory-induced sickness behavior.

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