Stress Response Mechanisms in Chronic Pain Sample Clauses

Stress Response Mechanisms in Chronic Pain. A dysregulation of the stress system in patients with chronic pain may be the result of several physiological mechanisms. A popular idea is that physical or emotional stressors overburden the stress response system, which ultimately ends in enhanced chronic pain (e.g., XxXxxx & Xxxxx, 2010; Xxxxx et al., 2012; Van Houdenhove et al., 2009; Woda et al., 2016). According to this view, enduring stress leads to hyper(re)activity of the stress system, which, in the long term, may induce functional or structural changes in receptors. Such changes may involve receptor downregulation or increased negative feedback, for example, leading to glucocorticoid receptor resistance. By losing the ability to flexibly respond to an ever-changing environment, disturbances in neurotransmitter functions, immunological mechanisms, and central pain processing may appear. Immune cells may become resistant to cortisol effects, leading to a chronic activation of pro-inflammatory cytokine production (Xxxxxxxxxxxx et al., 2005; Xxxxx et al., 2012). The resulting overactive immune-mediated sickness response may instigate a conglomerate of psychoneurobiological symptoms (Xxxxxxx et al., 2008; Xxxxx et al., 2012; XxXxxx & Xxxxx, 2010; Xxxxxxxxxxxx et al., 2005; Xxxxx & Xxxxx, 2016; Van Houdenhove & Luyten, 2009; Van Houdenhove et al., 2009; Woda et al., 2016). Thus, the overburdening of the stress system is one possible pathway that results in increased pain and reduced pain tolerance. Nonetheless, other pathways have been proposed to explain the association between early life stress and chronic pain. These include long-lasting changes in developing neurotransmitter and endocrine circuits linked to anxiety and stress, nociceptive circuitry, and stress responsivity in addition to genetic polymorphisms (p.187) and epigenetics (Xxxxxxx et al., 2008; Low & Schweinhardt, 2012; Woda et al., 2016). When we turn to the evidence in support of these ideas, a somewhat blurred picture emerges, with different studies reporting different findings regarding the activation of the stress system in patients with chronic pain. In support of the hyper(re)activity of the stress system, some studies have reported a hyper- reactivity in the ANS (e.g., decreased heart rate variability) and HPA-axis functioning in response to acute laboratory or naturalistic (chronic) stressors in patients with chronic pain (Xxxxxxx et al., 2008; Xxxxxx et al., 2006; Xxxxxx et al., 2016; XxXxxx & Xxxxx, 0000; Xxxxx & Clauw, 2016;...
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