4.4 Article

Associations Between Catastrophizing and Endogenous Pain-Inhibitory Processes: Sex Differences

期刊

JOURNAL OF PAIN
卷 10, 期 2, 页码 180-190

出版社

CHURCHILL LIVINGSTONE
DOI: 10.1016/j.jpain.2008.08.012

关键词

Diffuse noxious inhibitory controls; endogenous pain-inhibition; pain catastrophizing; sex differences

资金

  1. NCCIH NIH HHS [R21AT003250-01A1] Funding Source: Medline
  2. NIAMS NIH HHS [K23AR051315-01] Funding Source: Medline
  3. NINDS NIH HHS [R21NS48593] Funding Source: Medline

向作者/读者索取更多资源

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. (c) 2009 by the American Pain Society

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