Evidence from randomized controlled studies shows that reconceptualizing pain improves patients' knowledge of pain biology, reduces catastrophizing thoughts, and improves pain and function. However, causal relationships between these variables remain untested. It is hypothesized that reductions in catastrophizing could mediate the relationship between improvements in pain knowledge and improvements in pain and function. To test this causal mechanism, we conducted longitudinal mediation analyses on a cohort of 799 patients who were exposed to a pain education intervention. Patients provided responses to the neurophysiology of pain questionnaire, catastrophic thoughts about pain scale, visual analogue pain scale, and the patient specific functional scale, at baseline, 1-month, 6-month, and 12-month follow-up. With adjustment for potential confounding variables, an improvement in pain biology knowledge was significantly associated with a reduction in pain intensity (total effect = −2.20, 95% confidence interval [CI] = −2.96 to −1.44). However, this effect was not mediated by a reduction in catastrophizing (indirect effect = −0.16, 95% CI = −0.36 to 0.02). This might be due to a weak, nonsignificant relationship between changes in catastrophizing and pain intensity (path b = 0.19, 95% CI = −0.03 to 0.41). Similar trends were found in models with function as the outcome. Our findings indicate that change in catastrophizing did not mediate the effect of pain knowledge acquisition on change in pain or function. The strength of this conclusion is moderated, however, if patient-clinician relational factors are conceptualized as a consequence of catastrophizing, rather than a cause.
Supplemental Digital Content is Available in the Text.Explaining pain leads to long-term improvements in pain and function, but this effect is not mediated through changes in catastrophizing.
aNeuroscience Research Australia (NeuRA), Sydney, NSW, Australia
bPrince of Wales Clinical School, University of New South Wales, Sydney, NSW, Australia
cEMGO+ Institute, VU University Medical Centre, Amsterdam, the Netherlands
dThe George Institute for Global Health, University of Sydney, Sydney, NSW, Australia
eSansom Institute for Health Research, University of South Australia, Adelaide, SA, Australia
Corresponding author. Address: Sansom Institute for Health Research, GPO Box 2471, Adelaide 5001, Australia. Tel.: +610883022454. E-mail address: Lorimer.Moseley@unisa.edu.au (G.L. Moseley).
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Received August 31, 2015
Received in revised form November 13, 2015
Accepted December 11, 2015