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Mind–body interactions in pain: the neurophysiology of anxious and catastrophic pain-related thoughts

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The well-accepted biopsychosocial model proposes that the experience of pain and responses to it result from a complex interaction of biological, psychological, and social factors. However, the separation of these constructs is substantially artificial, and we presume that psychological processes have biological effects, that biological processes affect an individual's psychosocial environment, and so on. Considerable research has demonstrated that pain-coping strategies influence perceived pain intensity and physical functioning, and individual differences in styles of pain coping even shape the persistence of long-term pain complaints in some populations. A good deal of this coping research has focused on catastrophizing, which is a generally maladaptive cognitive and emotional mental set that involves feelings of helplessness when in pain, rumination about pain symptoms, and magnification of pain-related complaints. Collectively, catastrophizing has been consistently associated with heightened experiences of pain across a variety of samples. Although catastrophic thinking regarding pain-related symptoms is often classified under the “psychologic” category within the broader biopsychosocial model, we propose that catastrophizing exerts biologic effects that may account for some of its negative consequences. In general, the cognitive and affective processes captured within the construct of catastrophizing may exert effects on the neuromuscular, cardiovascular, immune, and neuroendocrine systems, and on the activity in the pain neuromatrix within the brain. The interface between pain-related neurobiology and processes such as pain-related catastrophizing represents an important avenue for future pain research.

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Functional neuroimaging studies: Catastrophizing in the brain

The advent of noninvasive functional neuroimaging methods that can be used to evaluate brain responses to noxious stimulation has to some degree revolutionized the field of pain research.5, 6, 7 Not surprisingly, such methods have been instrumental in demonstrating the “effects” of various psychologic processes (eg, attention or mood) on pain processing in the central nervous system. To date, 2 functional magnetic resonance imaging (fMRI) studies have shown, using application of standardized

Catastrophizing and opioid analgesic systems

Some developing evidence also suggests that high levels of catastrophizing may produce dysregulation or dysfunction in endogenous opioid pain-control systems. Endogenous opioids are central neurochemical players in multiple pain-inhibitory systems, and opioids such as beta-endophins act both in the periphery and in the central nervous system to modulate incoming information related to noxious stimulation. In several studies, elevated catastrophizing has been associated with a greater need for

Catastrophizing and inflammation

We recently reviewed the literature on catastrophizing's influence on pain in the context of rheumatic diseases,2 and we suggested that catastrophizing might be associated with activation of systemic inflammatory processes. For example, studies in patients with rheumatoid arthritis have reported positive associations between helplessness (a key component of catastrophizing) and elevated indices of inflammatory disease activity.18, 19, 20, 21, 22 Several of these investigations are longitudinal

Other physiologic parameters

Some other studies have provided evidence that catastrophizing may exert a broad influence on physiologic responses to pain, and that its influence may extend across multiple systems. For example, in several studies of healthy young adults, catastrophizing predicted increased systolic blood pressure reactivity to pain27 and enhanced myocardial contractility for a prolonged period of time following a cold pressor task.28 Relatedly, catastrophizing seems to influence the relationship among muscle

Catastrophizing and pain genetics

Examining the genetic contribution to disease states has become increasingly popular, and pain is no exception.37 To date, a handful of genetic polymorphisms has been linked with risk for chronic pain or with sensitivity to pain, as assessed in the laboratory.37 Although no published studies have yet described a genetic profile associated with catastrophizing, one recent report highlighted an intriguing interaction between catastrophizing and variability in the catechol-O-methyltransferase

Conclusions

Taken together, this literature provides demonstrative evidence for complex neuroendocrine, neuroimmune, psychophysiologic, and functional neuroanatomic “effects” of catastrophizing on the pain experience. Research that examines both physiological and psychosocial factors and how they shape long-term pain outcomes is an exciting area for future study and highlights the truly biopsychosocial nature of the pain experience. Future studies may wish to examine: (1) some potential molecular bases for

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    • Cited by (0)

    Supported by grants K23 AR051315 (to R.R.E.) and F32 NS063624 (to C.M.C.) from the National Institutes of Health, by awards from the American College of Rheumatology (to R.R.E.) and Arthritis Foundation (to R.R.E.), and by a collaborative research grant from the International Association for the Study of Pain.

    ∗

    Robert R. Edwards, PhD is a Lecturer on Anaesthesia at the Pain Management Center at Brigham and Women's Hospital. His article is based on a presentation given at the Combined Annual Meeting of the Central Society for Clinical Research and Midwestern Section American Federation for Medical Research held in Chicago, Ill, April 2008.

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