I know the pain you feel—how the human brain's default mode predicts our resonance to another's suffering (original) (raw)
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Dissociating anticipation from perception: Acute pain activates default mode network
Human Brain Mapping, 2012
Few studies have explored the effect of acute pain on attentional networks and on the default mode network. Moreover, these studies convey conflicting results, seemingly caused by design. To reassess this issue, we studied 20 healthy subjects with functional magnetic resonance imaging while delivering painful electric shocks. The design was purposely constructed to separate rest, anticipation, and pain perception. We found that default mode network activity in response to pain was biphasic. It deactivated during anticipation when the dorsal attentional network was activated. During pain perception, the default mode network was activated, as were attentional networks. The left posterior fusiform gyrus showed the same dynamics as the default mode network, and its activity was negatively correlated to the subject's pain intensity rating. The associative pregenual anterior cingulate cortex seemed to play a key role in these coactivations. These results concur with data from the literature showing that enhanced pain perception results in greater default mode network activity and that the anticorrelation between the default mode network and the dorsal attentional network disappears in chronic pain patients.
Frontiers in human neuroscience, 2017
Around a quarter of the population report "mirror pain" experiences in which bodily sensations of pain are elicited in response to viewing another person in pain. We have shown that this population of responders further fractionates into two distinct subsets (Sensory/localized and Affective/General), which presents an important opportunity to investigate the neural underpinnings of individual differences in empathic responses. Our study uses fMRI to determine how regions involved in the perception of pain interact with regions implicated in empathic regulation in these two groups, relative to controls. When observing pain in others (minor injuries to the hands and feet), the two responder groups show activation in both the sensory/discriminative and affective/motivational components of the pain matrix. The control group only showed activation in the latter. The two responder groups showed clear differences in functional connectivity. Notably, Sensory/Localized responders m...
Prior exposure to extreme pain alters neural response to pain in others
Cognitive, Affective, & Behavioral Neuroscience, 2016
In the extant literature examining the brain mechanisms implicated in pain perception, researchers have theorized that the overlapping responses to pain in the self and in others mark the human capacity for empathy. Here we investigated how prior exposure to extreme pain affects pain perception, by assessing the dynamics of pain processing in veterans who were previously exposed to severe injury. Fortythree participants (28 pain-exposed and 15 controls) underwent whole-head magnetoencephalography (MEG) while viewing photographs of limbs in painful and nonpainful (neutral) conditions. Among controls, an early (0-220 ms) Bpain effect^in the posterior cingulate and sensorimotor cortices, and a later (760-900 ms) Bpain effect^in the posterior cingulate cortex, superior temporal gyrus/insula, and fusiform gyrus were found, indicated by enhanced alpha suppression to the pain versus nonpain conditions. Importantly, pain-exposed participants exhibited an atypical pain response in the posterior cingulate cortex, indicated by a normative response to pain, but no pain-to-no-pain differentiation. This may suggest that individuals exposed to extreme pain may perceive neutral stimuli as potentially threatening. Our findings demonstrate alterations in pain perception following extreme pain exposure, chart the sequence from automatic to evaluative pain processing, and emphasize the importance of considering past experiences in studying the neural response to others' states. Keywords Pain perception. MEG. Alpha suppression. Posterior cingulate cortex Understanding how the brain processes the experience of pain has played a key role in the field of social neuroscience. Research on pain perception in one's self and others has not only identified the brain networks activated when humans experience pain, but also showed overlapping activations to pain within the self and others (Y. Fan, Duncan, de Greck, & Northoff, 2011; Lamm, Decety, & Singer, 2011). Such overlap between the first-and third-person perspectives has provided the basis for much theorizing (Bastiaansen, Thioux, & Keysers, 2009) and has highlighted the ability to represent others' states in one's own brain as the mechanism underpinning the human capacity for empathy (Decety & Sommerville, 2003; Feldman, 2015). The brain activation patterns associated with the first-hand experience of pain are well-defined, thus providing a reliable basis for comparing the brain response to pain in the self and others (Cheng, Yang, Lin, Lee, & Decety, 2008). Functional magnetic resonance imaging (fMRI) studies have repeatedly shown that both the first-hand experience of pain and the observation of pain in others activate regions of the insula, cingulate cortex (
Pain anticipation: An activation likelihood estimation meta-analysis of brain imaging studies
Human Brain Mapping, 2014
The anticipation of pain has been investigated in a variety of brain imaging studies. Importantly, today there is no clear overall picture of the areas that are involved in different studies and the exact role of these regions in pain expectation remains especially unexploited. To address this issue, we used activation likelihood estimation meta-analysis to analyze pain anticipation in several neuroimaging studies. A total of 19 functional magnetic resonance imaging were included in the analysis to search for the cortical areas involved in pain anticipation in human experimental models. During anticipation, activated foci were found in the dorsolateral prefrontal, midcingulate and anterior insula cortices, medial and inferior frontal gyri, inferior parietal lobule, middle and superior temporal gyrus, thalamus, and caudate. Deactivated foci were found in the anterior cingulate, superior frontal gyrus, parahippocampal gyrus and in the claustrum. The results of the meta-analytic connectivity analysis provide an overall view of the brain responses triggered by the anticipation of a noxious stimulus. Such a highly distributed perceptual set of self-regulation may prime brain regions to process information where emotion, action and perception as well as their related subcategories play a central role. Not only do these findings provide important information on the neural events when anticipating pain, but also they may give a perspective into nocebo responses, whereby negative expectations may lead to pain worsening. Hum Brain Mapp 36:1648-1661, 2015.
NeuroImage, 2011
Recent neuroimaging studies have revealed a persistent architecture of intrinsic connectivity networks (ICNs) in the signal of functional magnetic resonance imaging (fMRI) of humans and other species. ICNs are characterized by coherent ongoing activity between distributed brain regions during rest, in the absence of externally oriented behavior. While these networks strongly reflect anatomical connections, the relevance of ICN activity for human behavior remains unclear. Here, we investigated whether intrinsic brain activity adapts to repeated pain and encodes an individual's experience. Healthy subjects received a short episode of heat pain on 11 consecutive days. Across this period, subjects either habituated or sensitized to the painful stimulation. This adaptation was reflected in plasticity of a sensorimotor ICN (SMN) comprising pain related brain regions: coherent intrinsic activity of the somatosensory cortex retrospectively mirrored pain perception; on day 11, intrinsic activity of the prefrontal cortex was additionally synchronized with the SMN and predicted whether an individual would experience more or less pain during upcoming stimulation. Other ICNs of the intrinsic architecture remained unchanged. Due to the ubiquitous occurrence of ICNs in several species, we suggest intrinsic brain activity as an integrative mechanism reflecting accumulated experiences.
The Neural Mechanisms of Social Learning from Fleeting Experience with Pain
Frontiers in Behavioral Neuroscience, 2016
Social learning is critical for humans to adapt and cope with rapidly changing surroundings. Although, neuroscience has focused on associative learning and pain empathy, the neural mechanisms of social learning through fleeting pain remains to be determined. This functional MRI study included three participant groups, to investigate how the neuro-hemodynamic response and subjective evaluation in response to the observation of hand actions were modulated by first-hand experience (FH), as well as indirect experience through social-observational (SO), and verbal-informed (VI) learning from fleeting pain. The results indicated, that these three learning groups share the common neuro-hemodynamic activations in the brain regions implicated in emotional awareness, memory, mentalizing, perspective taking, and emotional regulation. The anterior insular cortex (AIC) was commonly activated during these learning procedures. The amygdala was only activated by the FH. Dynamic causal modeling further indicated, that the SO and VI learning exhibited weaker connectivity strength from the AIC to superior frontal gyrus than did the FH. These findings demonstrate, that social learning elicits distinct neural responses from associative learning. The ontogeny of human empathy could be better understood with social learning from fleeting experience with pain.
Mind wandering away from pain dynamically engages antinociceptive and default mode brain networks
Proceedings of the National Academy of Sciences, 2013
Human minds often wander away from their immediate sensory environment. It remains unknown whether such mind wandering is unsystematic or whether it lawfully relates to an individual's tendency to attend to salient stimuli such as pain and their associated brain structure/function. Studies of pain-cognition interactions typically examine explicit manipulation of attention rather than spontaneous mind wandering. Here we sought to better represent natural fluctuations in pain in daily life, so we assessed behavioral and neural aspects of spontaneous disengagement of attention from pain. We found that an individual's tendency to attend to pain related to the disruptive effect of pain on his or her cognitive task performance. Next, we linked behavioral findings to neural networks with strikingly convergent evidence from functional magnetic resonance imaging during pain coupled with thought probes of mind wandering, dynamic resting state activity fluctuations, and diffusion MRI. We found that (i) pain-induced default mode network (DMN) deactivations were attenuated during mind wandering away from pain; (ii) functional connectivity fluctuations between the DMN and periaqueductal gray (PAG) dynamically tracked spontaneous attention away from pain; and (iii) across individuals, stronger PAG-DMN structural connectivity and more dynamic resting state PAG-DMN functional connectivity were associated with the tendency to mind wander away from pain. These data demonstrate that individual tendencies to mind wander away from pain, in the absence of explicit manipulation, are subserved by functional and structural connectivity within and between default mode and antinociceptive descending modulation networks.
Although social and physical pain recruit overlapping neural activity in regions associated with the affective component of pain, the two pains can diverge in their phenomenology. Most notably, feelings of social pain can be re-experienced or "relived," even when the painful episode has long passed, whereas feelings of physical pain cannot be easily relived once the painful episode subsides. Here, we observed that reliving social (vs. physical) pain led to greater self-reported re-experienced pain and greater activity in affective pain regions (dorsal anterior cingulate cortex and anterior insula). Moreover, the degree of relived pain correlated positively with affective pain system activity. In contrast, reliving physical (vs. social) pain led to greater activity in the sensory-discriminative pain system (primary and secondary somatosensory cortex and posterior insula), which did not correlate with relived pain. Preferential engagement of these different pain mechanisms may reflect the use of different top-down neurocognitive pathways to elicit the pain. Social pain reliving recruited dorsomedial prefrontal cortex, often associated with mental state processing, which functionally correlated with affective pain system responses. In contrast, physical pain reliving recruited inferior frontal gyrus, known to be involved in body state processing, which functionally correlated with activation in the sensory pain system. These results update the physical-social pain overlap hypothesis: while overlapping mechanisms support live social and physical pain, distinct mechanisms guide internally-generated pain.
Neural Correlates of Empathy with Pain Show Habituation Effects. An fMRI Study
PLOS ONE, 2015
Neuroimaging studies have demonstrated that the actual experience of pain and the perception of another person in pain share common neural substrates, including the bilateral anterior insular cortex and the anterior midcingulate cortex. As many fMRI studies include the exposure of participants to repeated, similar stimuli, we examined whether empathic neural responses were affected by habituation and whether the participants' prior pain experience influenced these habituation effects.
Functional connectivity of the frontoparietal network predicts cognitive modulation of pain
Pain, 2013
The experience of pain can be significantly influenced by expectancy (predictive cues). This ability to modulate pain has the potential to affect therapeutic analgesia substantially and constitutes a foundation for non-pharmacological pain relief. In this study, we investigated 1) brain regions involved in visual cue modulation of pain during anticipation of pain, pain administration, and pain rating; and 2) the association between pre-test resting-state functional connectivity and the magnitude of cue effects on pain ratings. We found that after cue conditioning, visual cues can significantly modulate subjective pain ratings. fMRI results suggested that brain regions pertaining to the frontoparietal network (prefrontal and parietal cortex) and a pain/emotion modulatory region (rostral anterior cingulate cortex, rACC) are involved in cue modulation during both pain anticipation and administration stage. Most interestingly, we found that pre-test resting state functional connectivity between the frontoparietal network (as identified by independent component analysis) and the rACC/MPFC was positively associated with cue effects on pain rating changes. We believe that these finding will shed new light on our understanding of variable cue/expectancy effects across individuals and how the intrinsic connectivity of the brain may influence expectancy induced modulation of pain.