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      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

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          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.

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          Most cited references149

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          Central sensitization: implications for the diagnosis and treatment of pain.

          Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity. Copyright © 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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            Stress, memory and the amygdala.

            Emotionally significant experiences tend to be well remembered, and the amygdala has a pivotal role in this process. But the efficient encoding of emotional memories can become maladaptive - severe stress often turns them into a source of chronic anxiety. Here, we review studies that have identified neural correlates of stress-induced modulation of amygdala structure and function - from cellular mechanisms to their behavioural consequences. The unique features of stress-induced plasticity in the amygdala, in association with changes in other brain regions, could have long-term consequences for cognitive performance and pathological anxiety exhibited in people with affective disorders.
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              The prefrontal cortex (PFC) - the most evolved brain region - subserves our highest-order cognitive abilities. However, it is also the brain region that is most sensitive to the detrimental effects of stress exposure. Even quite mild acute uncontrollable stress can cause a rapid and dramatic loss of prefrontal cognitive abilities, and more prolonged stress exposure causes architectural changes in prefrontal dendrites. Recent research has begun to reveal the intracellular signalling pathways that mediate the effects of stress on the PFC. This research has provided clues as to why genetic or environmental insults that disinhibit stress signalling pathways can lead to symptoms of profound prefrontal cortical dysfunction in mental illness.
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                Author and article information

                Contributors
                Journal
                Front Psychol
                Front Psychol
                Front. Psychol.
                Frontiers in Psychology
                Frontiers Media S.A.
                1664-1078
                23 March 2021
                2021
                : 12
                : 630422
                Affiliations
                [1] 1The Mind-Body Lab, Department of Psychology, Faculty of Social Sciences, University of Oslo , Oslo, Norway
                [2] 2Department of Pain Management and Research, Oslo University Hospital , Oslo, Norway
                Author notes

                Edited by: Julie Lasselin, Karolinska Institutet (KI), Sweden

                Reviewed by: Sven Benson, Essen University Hospital, Germany; Mats Lekander, Karolinska Institutet (KI), Sweden

                *Correspondence: Henrik Børsting Jacobsen, henrbors@ 123456uio.no

                This article was submitted to Health Psychology, a section of the journal Frontiers in Psychology

                Article
                10.3389/fpsyg.2021.630422
                8023326
                ddd70796-ff09-4564-bc35-2071599c25b6
                Copyright © 2021 Munk, Reme and Jacobsen.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 17 November 2020
                : 01 March 2021
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 149, Pages: 14, Words: 12810
                Funding
                Funded by: Norwegian Cancer Society 10.13039/100008730
                Categories
                Psychology
                Review

                Clinical Psychology & Psychiatry
                breast cancer,chronic postsurgical pain,cognitive activation theory of stress,expectancies,sickness behavior,stress,predictive coding,hypnosis

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