Cold pressor pain and psychophysiological activation in high and low pain catastrophizers

Abstract

Pain catastrophizing is a robust predictor of heightened pain report. However, theoretical models addressing mechanisms of catastrophizing are lacking. The purpose of this study was to examine whether high and low catastrophizers manifest differential psychophysiological arousal patterns in an experimental laboratory pain setting. Gender differences and covariates were also examined. Participants were 102 undergraduate students (56 female, 46 male) at Queen’s University recruited from the Psychology 100 subject pool aged 17-28 years (M = 18.44, SD = 1.40). After deleting participants with missing data, n = 95 for pain report/psychological variables, and n = 93 for psychophysiological measures. Participants were pre-screened using the Pain Catastrophizing Scale (PCS) from which individuals were selected from the top third (i.e., PCS score ≥ 24) and the bottom third (i.e., PCS score ≤ 13) of the distribution to represent high and low catastrophizers respectively. Participants completed measures of depression and anxiety before participating in a cold pressor task. Participants’ heart rate (HR) and galvanic skin response (GSR) were recorded during periods of baseline (3 minutes), pain induction (1 minute), and pain recovery (10 minutes). The Short-Form McGill Pain Questionnaire (SF-MPQ) was completed following the recovery period. Results showed that catastrophizing was related to greater pain intensity during pain induction and during pain recovery, as well as greater retrospective sensory and affective reports of pain. Women reported greater pain intensity during pain induction, during pain recovery, and greater retrospective reports of sensory pain. These effects were significant even when controlling for depression and anxiety. With regard to psychophysiological arousal, catastrophizing was related to higher HR during pain induction. There also appeared to be trends suggesting that catastrophizing may also be associated with HR before and after pain induction. Results provide partial support for an appraisal model of catastrophizing and may be useful in informing future models implicating catastrophizing in the development and maintenance of chronic pain.