TY - JOUR
T1 - Mind-body interactions in pain
T2 - the neurophysiology of anxious and catastrophic pain-related thoughts
AU - Campbell, Claudia M.
AU - Edwards, Robert R.
N1 - Funding Information:
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.
PY - 2009/3
Y1 - 2009/3
N2 - 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.
AB - 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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U2 - 10.1016/j.trsl.2008.12.002
DO - 10.1016/j.trsl.2008.12.002
M3 - Review article
C2 - 19218091
AN - SCOPUS:59849106618
VL - 153
SP - 97
EP - 101
JO - Translational Research
JF - Translational Research
SN - 1931-5244
IS - 3
ER -