Empathy for pain activates brain areas partially overlapping with those underpinning the first-hand experience of pain. It remains unclear, however, whether such shared activations imply that pain empathy engages similar neural functions as first-hand pain experiences. To overcome the limitations of previous neuroimaging research, we pursued a conceptually novel approach: we used the phenomenon of placebo analgesia to experimentally reduce the first-hand experience of pain, and assessed whether this results in a concomitant reduction of empathy for pain. We first carried out a functional MRI experiment (n = 102) that yielded results in the expected direction: participants experiencing placebo analgesia also reported decreased empathy for pain, and this was associated with reduced engagement of anterior insular and midcingulate cortex: that is, areas previously associated with shared activations in pain and empathy for pain. In a second step, we used a psychopharmacological manipulation (n = 50) to determine whether these effects can be blocked via an opioid antagonist. The administration of the opioid antagonist naltrexone blocked placebo analgesia and also resulted in a corresponding “normalization” of empathy for pain. Taken together, these findings suggest that pain empathy may be associated with neural responses and neurotransmitter activity engaged during first-hand pain, and thus might indeed be grounded in our own pain experiences.

Previous research in social neuroscience has consistently shown that empathy for pain recruits brain areas that are also activated during the first-hand experience of pain. This has been interpreted as evidence that empathy relies upon neural processes similar to those underpinning the first-hand experience of emotions. However, whether such overlapping neural activations imply that equivalent neural functions are engaged by empathy and direct emotion experiences remains to be demonstrated. We induced placebo analgesia, a phenomenon specifically modulating the first-hand experience of pain, to test whether this also reduces empathy for pain. Subjective and neural measures of pain and empathy for pain were collected using self-report and event-related potentials (ERPs) while participants underwent painful electrical stimulation or witnessed that another person was undergoing such stimulation. Self-report showed decreased empathy during placebo analgesia, and this was mirrored by reduced amplitudes of the pain-related P2, an ERP component indexing neural computations related to the affective-motivational component of pain. Moreover, these effects were specific for pain, as self-report and ERP measures of control conditions unrelated to pain were not affected by placebo analgesia. Together, the present results suggest that empathy seems to rely on neural processes that are (partially) functionally equivalent to those engaged by first-hand emotion experiences. Moreover, they imply that analgesics may have the unwanted side effect of reducing empathic resonance and concern for others.

There is evidence that development and maintenance of neural connections are disrupted in major mental disorders, which indicates that neurotrophic factors could play a critical role in their pathogenesis. Stress is a well-established risk factor for psychopathology and recent research suggests that disrupted signaling via brain-derived neurotrophic factor (BDNF) may be involved in mediating the negative effects of stress on the brain. Social isolation of rats elicits chronic stress and is widely used as an animal model of mental disorders such as schizophrenia and depression. We carried out a systematic search of published studies to review current evidence for an altered expression of BDNF in the brain of rats reared or housed social isolation. Across all age groups (postweaning, adolescent, adult), majority of the identified studies (16/21) reported a decreased expression of BDNF in the hippocampus. There are far less published data on BDNF expression in other brain regions. Data are also scarce to assess the behavioral changes as a function of BDNF expression, but the downregulation of BDNF seems to be associated with increased anxiety-like symptoms. The reviewed data generally support the putative involvement of BDNF in the pathogenesis of stress-related mental illness. However, the mechanisms linking chronic social isolation, BDNF expression and the elicited behavioral alterations are currently unknown.

People evaluate members of their own social group more favorably and empathize more strongly with their ingroup members. Using electroencephalography (EEG), we explored whether resonant responses of sensorimotor cortex to the pain of others are modulated by the ethnicity of these others. White participants watched video clips of ethnic ingroup and outgroup hands, being either penetrated by a needle syringe or touched by a cotton swab, while EEG was recorded. Time-frequency analysis was applied to Laplacian-transformed signals from the sensors overlying sensorimotor cortex in order to assess event-related desynchronization and synchronization (ERD/ERS) of sensorimotor mu (7–12 Hz) and beta (13–30 Hz) rhythms. When watching needle injections, beta ERD was significantly stronger for ingroup compared with outgroup hands. This ethnicity bias was restricted to painful actions, as beta ERD for ingroup and outgroup hands neither differed when observing no-pain videos, nor during presentation of the hands without any treatment. Such vicarious sensorimotor activation could play a role in social interaction by enhancing the understanding of the feelings and reactions of others and hence facilitating behavioral coordination among group members.

Pain is a salient, aversive sensation which motivates avoidance, but also has a strong social signaling function. Numerous studies have shown that regions of the nervous system active in association with first-hand pain are also active in response to the pain of others. When witnessing somatic pain, such as seeing bodies in painful situations, significant activations occur not only in areas related to the processing of negative emotions, but also in neuronal structures engaged in somatosensation and the control of skeletal muscles. These empathy-related sensorimotor activations are selectively reviewed in this article, with a focus on studies using electrophysiological methods and paradigms investigating responses to somatic pain. Convergent evidence from these studies shows that these activations (1) occur at multiple levels of the nervous system, from the spinal cord up to the cerebral cortex, (2) are best conceptualized as activations of a defensive system, in line with the role of pain to protect body from injury, and (3) contribute to establishing a matching of psychological states between the sufferer and the observer, which ultimately supports empathic understanding and motivate prosocial action. Future research should thus focus on how these sensorimotor responses are related to higher-order empathic responses, including affective sharing and emotion regulation, and how this motivates approach-related prosocial behaviors aimed at alleviating the pain and suffering of others.