Processes linking pain catastrophizing to adverse pain outcomes
An appraisal conceptualization of pain catastrophizing suggests several cognitive and emotional processes through which pain catastrophizing might impact on pain experience. These might include expectancies, attentional mechanisms, emotional distress states and the mobilization of distress reduction strategies (i.e. coping strategies). Research examining the role of these variables as determinants of the relation between pain catastrophizing and pain outcomes will be briefly reviewed.
Expectancies are essentially an individual’s predictions about the future. In pain research, researchers have distinguished between ‘response expectancies’ and ‘efficacy expectancies’ (Bandura 1977; Kirsch 1985). Predictions about non-volitional responses to a particular stimulus are referred to as ‘response expectancies’. Efficacy expectancies (e.g. self-efficacy) refer to the confidence individuals’ have that they possess the ability to successfully execute the behaviour required to yield a desired outcome (Bandura 1977). Considerable research has shown that there is a high degree of concordance between pain expectancies and pain experience (Jensen et al. 1991a; Lacker et al. 1996).
Response expectancies for pain have been discussed as a significant determinant of actual pain experience (Crombez et al. 1996; Jensen et al. 1991a). For example, the powerful analgesic effects of placebos have been discussed in terms of expectancy manipulations (Pollo et al. 2001; Whalley et al. 2008). It has been suggested that many psychological interventions for pain management may exert their effects, at least in part, through their influence on pain expectancies (Milling et al. 2006; Milling et al. 2007).
Research has provided support for a relation between pain catastrophizing and response expectancies. In an experimental study, Sullivan et al (Sullivan et al. 2001a) reported that pain catastrophizing was associated with expectancies for heightened pain and emotional distress. Van Damme et al (Van Damme et al. 2002) also found a significant relation between pain catastrophizing and pain expectancies and suggested that the pain expectancies of high pain catastrophizers might promote hypervigilance to pain signals. Not only do high pain catastrophizers expect to experience more pain, but there are findings to suggest that high pain catastrophizers fail to correct their pain expectancies in the face of disconfirming evidence (Crombez et al. 2002; Van Damme et al. 2002).
A number of investigations have shown a close association between self-efficacy expectancies and pain catastrophizing (Keefe et al. 1997b; Thorn et al. 2007). For example, scale items that assess self-efficacy for coping with pain have frequently loaded on the same factor as scale items that assess catastrophic thinking (Sullivan et al. 2001b). Albeit a close association, the two constructs do not appear to be redundant. One investigation revealed that self-efficacy prospectively predicted pain behaviour and activity avoidance, even when controlling for pain catastrophizing (Asghari and Nicholas 2001). In a recent study of patients with osteoarthritis, Shelby et al. (2008) found that domain-specific self-efficacy mediated the relation between pain catastrophizing and pain intensity.
There are indications that the impact of expectancies on pain outcomes might be unmediated (at least with respect to psychological variables). Kirsch (1985) has proposed that response expectancies may represent one of the most basic psychological variables. This position has significant implications for explicating the underlying basis of several psychological determinants of pain experience. Expectancies may represent the final common pathway of several psychological influences on pain perception.
Research suggests that similar brain regions might modulate the effects of pain catastrophizing and pain expectancies (Gracely et al. 2004; Ploghaus et al. 2003; Ploghaus et al. 1999). In addition, there are indications that catastrophizing and expectancies might exert influence on endogenous opioid mechanisms (Peyron et al. 2000). For example, it has been shown that the analgesic effects of high self-efficacy can be blocked with naloxone (i.e. an opioid antagonist) (Bandura et al. 1987). High levels of pain catastrophizing have been associated with poorer response to opioids for both clinical and experimental pain (Fillingim et al. 2005; Haythornthwaite et al. 2003; Jacobsen and Butler 1996).