Literature DB >> 19010738

Associations between catastrophizing and endogenous pain-inhibitory processes: sex differences.

Burel R Goodin1, Lynanne McGuire, Mark Allshouse, Laura Stapleton, Jennifer A Haythornthwaite, Noel Burns, Lacy A Mayes, Robert R Edwards.   

Abstract

UNLABELLED: Pain catastrophizing is among the most robust predictors of pain outcomes, and a disruption in endogenous pain-inhibitory systems is 1 potential mechanism that may account for increased pain among individuals who report higher pain catastrophizing. Pain catastrophizing may negatively influence diffuse noxious inhibitory controls (DNIC), a measure of endogenous pain inhibition, through complex anatomical circuitry linking cortical responses to pain with processes that modulate pain. The current study examined whether DNIC mediated the relationship between catastrophizing and pain among 35 healthy young adults and examined the moderating effects of sex to determine whether the magnitude or direction of associations differed among men and women. DNIC was assessed using pressure pain thresholds on the forearm before and during a cold pressor task. Using bias-corrected bootstrapped confidence intervals, results showed that diminished DNIC was a significant partial mediator of the relation between greater pain-related catastrophizing and more severe pain ratings. Participant sex moderated these associations; higher catastrophizing predicted lower DNIC for men and women, however, the effect of catastrophizing on pain ratings was partially mediated by DNIC for women only. These findings further support the primary role of pain catastrophizing in modulation of pain outcomes. PERSPECTIVE: These findings support the hypothesis that the heightened pain reported by individuals higher in pain catastrophizing may be related to a disruption in the endogenous modulation of pain, operationalized by assessing DNIC. Whether interventions that reduce pain catastrophizing affect pain outcomes via effects on DNIC is in need of investigation.

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Year:  2008        PMID: 19010738     DOI: 10.1016/j.jpain.2008.08.012

Source DB:  PubMed          Journal:  J Pain        ISSN: 1526-5900            Impact factor:   5.820


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