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Review
, 74 (2), 126-35

The Neural Bases of Social Pain: Evidence for Shared Representations With Physical Pain

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Review

The Neural Bases of Social Pain: Evidence for Shared Representations With Physical Pain

Naomi I Eisenberger. Psychosom Med.

Abstract

Experiences of social rejection or loss have been described as some of the most "painful" experiences that we, as humans, face and perhaps for good reason. Because of our prolonged period of immaturity, the social attachment system may have co-opted the pain system, borrowing the pain signal to prevent the detrimental consequences of social separation. This review summarizes a program of research that has explored the idea that experiences of physical pain and social pain rely on shared neural substrates. First, evidence showing that social pain activates pain-related neural regions is reviewed. Then, studies exploring some of the expected consequences of such a physical pain-social pain overlap are summarized. These studies demonstrate that a) individuals who are more sensitive to one kind of pain are also more sensitive to the other and b) factors that increase or decrease one kind of pain alter the other in a similar manner. Finally, what these shared neural substrates mean for our understanding of socially painful experience is discussed.

Figures

Figure 1
Figure 1
A conceptual model depicting the overlapping neural regions activated by physical and social pain as well as the consequences of this overlap for trait differences in sensitivity to pain (individual differences in physical pain sensitivity should correlate positively with individual differences in social pain sensitivity) and for state differences in sensitivity to pain (factors that increase or decrease one kind of pain should alter the other kind of pain in a congruent manner).
Figure 2
Figure 2
(A) Neural activity in the dACC that was greater during social exclusion vs. inclusion. (B) Correlation between dACC activity and self-reported social distress. (Adapted from Eisenberger et al., 2003.)
Figure 3
Figure 3
Neural activity (during exclusion vs. inclusion) that was greater for G allele carriers than A allele homozygotes in the (A) dACC and (B) anterior insula (p<.001, 20 voxels). C) Parameter estimates from the dACC (8,12,44; t(24)= 4.06, p< 0.001); D) Parameter estimates from the left anterior insula (−22,24, −8; t(24)= 5.07, p < 0.001). * denotes G allele homozygote. (Reprinted from Way et al., 2009.)
Figure 4
Figure 4
Neural activity (during exclusion vs. inclusion) that was greater for participants who took placebo (vs. those who took acetaminophen) in the dACC and right anterior insula (p < .005, 20 voxels). Bar graphs (with standard error bars) for each region show the activity during exclusion compared to inclusion, averaged across the entire cluster, for the acetaminophen and placebo groups. (Reprinted from DeWall et al., 2010.)

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