The phenomenon of empathy entails the ability to share the affective experiences of others. In recent years social neuroscience made considerable progress in revealing the mechanisms that enable a person to feel what another is feeling. The present review provides an in-depth and critical discussion of these findings. Consistent evidence shows that sharing the emotions of others is associated with activation in neural structures that are also active during the first-hand experience of that emotion. Part of the neural activation shared between self- and other-related experiences seems to be rather automatically activated. However, recent studies also show that empathy is a highly flexible phenomenon, and that vicarious responses are malleable with respect to a number of factors—such as contextual appraisal, the interpersonal relationship between empathizer and other, or the perspective adopted during observation of the other. Future investigations are needed to provide more detailed insights into these factors and their neural underpinnings. Questions such as whether individual differences in empathy can be explained by stable personality traits, whether we can train ourselves to be more empathic, and how empathy relates to prosocial behavior are of utmost relevance for both science and society.
The experience of pain occurs when the level of a stimulus is sufficient to elicit a marked affective response, putatively to warn the organism of potential danger and motivate appropriate behavioral responses. Understanding the biological mechanisms of the transition from innocuous to painful levels of sensation is essential to understanding pain perception as well as clinical conditions characterized by abnormal relationships between stimulation and pain response. Thus, the primary objective of this study was to characterize the neural response associated with this transition and the correspondence between that response and subjective reports of pain. Towards this goal, this study examined BOLD response profiles across a range of temperatures spanning the pain threshold. 14 healthy adults underwent functional magnetic resonance imaging (fMRI) while a range of thermal stimuli (44-49°C) were applied. BOLD responses showed a sigmoidal profile along the range of temperatures in a network of brain regions including insula and mid-cingulate, as well as a number of regions associated with motor responses including ventral lateral nuclei of the thalamus, globus pallidus and premotor cortex. A sigmoid function fit to the BOLD responses in these regions explained up to 85% of the variance in individual pain ratings, and yielded an estimate of the temperature of steepest transition from non-painful to painful heat that was nearly identical to that generated by subjective ratings. These results demonstrate a precise characterization of the relationship between objective levels of stimulation, resulting neural activation, and subjective experience of pain and provide direct evidence for a neural mechanism supporting the nonlinear transition from innocuous to painful levels along the sensory continuum.
Most of the extant literature investigating the health effects of mindfulness interventions relies on wait-list control comparisons. The current article specifies and validates an active control condition, the Health Enhancement Program (HEP), thus providing the foundation necessary for rigorous investigations of the relative efficacy of Mindfulness Based Stress Reduction (MBSR) and for testing mindfulness as an active ingredient. 63 participants were randomized to either MBSR (n = 31) or HEP (n = 32). Compared to HEP, MBSR led to reductions in thermal pain ratings in the mindfulness- but not the HEP-related instruction condition (η(2) = .18). There were significant improvements over time for general distress (η(2) = .09), anxiety (η(2) = .08), hostility (η(2) = .07), and medical symptoms (η(2) = .14), but no effects of intervention. Practice was not related to change. HEP is an active control condition for MBSR while remaining inert to mindfulness. These claims are supported by results from a pain task. Participant-reported outcomes (PROs) replicate previous improvements to well-being in MBSR, but indicate that MBSR is no more effective than a rigorous active control in improving these indices. These results emphasize the importance of using an active control condition like HEP in studies evaluating the effectiveness of MBSR.
Recent neuroimaging and neuropsychological work has begun to shed light on how the brain responds to the viewing of facial expressions of emotion. However, one important category of facial expression that has not been studied on this level is the facial expression of pain. We investigated the neural response to pain expressions by performing functional magnetic resonance imaging (fMRI) as subjects viewed short video sequences showing faces expressing either moderate pain or, for comparison, no pain. In alternate blocks, the same subjects received both painful and non-painful thermal stimulation. Facial expressions of pain were found to engage cortical areas also engaged by the first-hand experience of pain, including anterior cingulate cortex and insula. The reported findings corroborate other work in which the neural response to witnessed pain has been examined from other perspectives. In addition, they lend support to the idea that common neural substrates are involved in representing one's own and others' affective states.
Facial expressions of pain are an important part of the pain response, signaling distress to others and eliciting social support. To evaluate how voluntary modulation of this response contributes to the pain experience, 29 subjects were exposed to thermal stimulation while making standardized pain, control, or relaxed faces. Dependent measures were self-reported negative effect (valence and arousal) as well as the intensity of nociceptive stimulation required to reach a given subjective level of pain. No direct social feedback was given by the experimenter. Although the amount of nociceptive stimulation did not differ across face conditions, subjects reported more negative effects in response to painful stimulation while holding the pain face. Subsequent analyses suggested the effects were not due to preexisting differences in the difficulty or unpleasantness of making the pain face. These results suggest that voluntary pain expressions have no positively reinforcing (pain attenuating) qualities, at least in the absence of external contingencies such as social reinforcement, and that such expressions may indeed be associated with higher levels of negative affect in response to similar nociceptive input. PERSPECTIVE: This study demonstrates that making a standardized pain face increases negative affect in response to nociceptive stimulation, even in the absence of social feedback. This suggests that exaggerated facial displays of pain, although often socially reinforced, may also have unintended aversive consequences.