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Sex, Gender, and Pain: A Review of Recent Clinical and Experimental Findings http://psycnet.apa.org/index.cfm?fa=buy.

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Roger B. Fillingim , Christopher D. King, Margarete C. Ribeiro-Dasilva, Bridgett RahimWilliams, Joseph L. Riley III

Abstract Abstract Sex-related influences on pain and analgesia have become a topic of tremendous scientific and clinical interest, especially in the last 10 to 15 years. Members of our research group published reviews of this literature more than a decade ago, and the intervening time period has witnessed robust growth in research regarding sex, gender, and pain. Therefore, it seems timely to revisit this literature. Abundant evidence from recent epidemiologic studies clearly demonstrates that women are at substantially greater risk for many clinical pain conditions, and there is some suggestion that postoperative and procedural pain may be more severe among women than men. Consistent with our previous reviews, current human findings regarding sex differences in experimental pain indicate greater pain sensitivity among females compared with males for most pain modalities, including more recently implemented clinically relevant pain models such as temporal summation of pain and intramuscular injection of algesic substances. The evidence regarding sex differences in laboratory measures of endogenous pain modulation is mixed, as are findings from studies using functional brain imaging to ascertain sex differences in pain-related cerebral activation. Also inconsistent are findings regarding sex differences in responses to pharmacologic and non-pharmacologic pain treatments. The article concludes with a discussion of potential biopsychosocial mechanisms that may underlie sex differences in pain, and considerations for future research are discussed. Perspective This article reviews the recent literature regarding sex, gender, and pain. The growing body of evidence that has accumulated in the past 10 to 15 years continues to indicate substantial sex differences in clinical and experimental pain responses, and some evidence suggests that pain treatment responses may differ for women versus men.

Associations Between Catastrophizing and Endogenous Pain-Inhibitory Processes: Sex Differences http://www.jpain.org/article/S15265900(08)00739-6/fulltext
Burel R. Goodin, Lynanne McGuire , Mark Allshouse, Laura Stapleton, Jennifer A. Haythornthwaite, Noel Burns, Lacy A. Mayes, Robert R. Edwards Received 28 February 2008; received in revised form 8 August 2008; accepted 25 August 2008. published online 17 November 2008.

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Abstract
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.