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Endogenous pain inhibition does not appear to be the mechanism responsible for pregnancy-induced analgesia
Abstract Number: GM-2
Abstract Type: Original Research
Pregnancy-induced analgesia (PIA) is a well-described pain modulation phenomenon occurring during pregnancy. It is postulated that PIA occurs due to enhanced endogenous noxious inhibition and helps women tolerate the intense pain of labor. The aim of this study was to assess the hypothesis that endogenous noxious inhibition, as tested by diffuse noxious inhibitory controls (DNIC), would increase over the course of pregnancy, and that pregnant women would show greater inhibition compared to non-pregnant women.
A total of 31 pregnant (P) and 30 non-pregnant women (NP) were enrolled in this prospective, multicenter study. P women were assessed once each trimester (8-12wks, 18-22wks, at 36wks) and at 6-12wks postpartum. NP were assessed during 4 menstrual cycles (average score pre/post-ovulation) and compared with the P women visit scores. DNIC was performed as previously described (1). A 4x2 mixed design ANOVA was conducted to assess differences within and across subjects, with time (1-4) and group (P vs. NP) as independent variables, and DNIC as dependent variable. Intra-class correlation coefficients (ICC) were also calculated within each group to explore stability across time.
Overall, P women had less efficient DNIC compared to NP controls (F1,35 =5.23, p< .05; Fig). DNIC scores did not change significantly over time (F3, 35 =.84, p=.48), and there was no significant group by time interaction (F3,35 =0.53, p=.47). ICC for DNIC were significant for NP women (ICC=.60, p<.001), but not for P women (ICC=.03, p=.36), and there was greater variation in DNIC during pregnancy compared to controls.
This is the first study to assess DNIC changes in pregnancy. Contrary to our hypothesis, DNIC was less efficient in pregnant compared to non-pregnant women, and there were no significant changes in DNIC over time. There was less stability in DNIC among the pregnant group as compared to controls, suggesting that pregnancy may have some impact on DNIC. This variability also suggests sub-groups may exist that experience differential DNIC response throughout pregnancy. These negative findings may reflect that PIA is not driven by enhanced endogenous noxious inhibition, however we cannot exclude the possibility that it may play a role in combination with other effects that were not tested.
1. J Vis Exp. 2010 Jan 27;(35)