Empathy refers to one's emotional state that is elicited by, and isomorphic to, another person's emotional state, with a clear self-other distinction. Painful situations are the most commonly used triggers for eliciting empathy. Numerous neuroimaging studies have shown that exposure to another’s pain can activate brain regions that overlap those involved in the direct experience of pain, including anterior insula and anterior/middle cingulate cortex. This shared neural activation is called a 'shared representation' account. Another line of research has focused on various factors that modulate shared neural representation during empathy, including observer and sufferer characteristics, the relationship between the empathy dyad, and the contextual factors. Although the neural underpinnings of pain empathy have been extensively studied, the phenomenological observation has been poorly investigated. It remains unclear how the modulation of pain empathy elicited by above-mentioned factors occur .
Emotional mimicry is defined as an automatic tendency to match another one's emotional state in social interaction. By imitating a facial expression of others, we have direct access to the emotion that trigger the facial expression. Some investigators argue that emotional mimicry may precede empathy. There is also solid evidence that inhibiting or facilitating facial mimicry have an impact on the perception and understanding of other's emotion. Hence, emotional mimicry may be the phenomenological signature of empathy.
The present doctorial project involved 3 studies, aiming to address these issues. Study 1 examined observers' emotional mimicry when they watched video clips depicting painful scenes using facial electromyography (EMG) recording method. Enhanced EMG activity of the corrugator supercilii (CS) and zygomaticus major (ZM) muscles was found when observers viewed others in pain, supporting a unique pain expression that is distinct from the expression of basic emotions. CS activity was positively correlated with the empathic concern score as well as ZM activity, suggesting a facial mimicry that mediated empathy for pain. The results demostrated that emotional mimicry can serve as a phenomenological signature of empathy.
To clarify the causal contribution of emotional mimicry in pain empathy, two experiments were designed in study 2 in laboratory and clinical settings respectively. Experiment 1 adopted a 5 (group: blank control, negative control, pen-biting inhibition, plastic bandage inhibition, and voluntary imitation) × 2 (condition: pain vs. No-pain) mixed model design. The results showed that, compared to control groups, imitation group showed more sympathy towards others in pain, whereas inhibition manipulations had no influence on empathy reactions. Experiment 2 investigated the impact of facial mimicry disturbance on empathy for pain in hemifacial spasm (HFS) patients. Facial EMG indicated that healthy controls (HCs) showed a normal, typical emotional mimicry activity when facing others in pain, whereas HFS patients showed involuntary facial twitching during most of the experimental trials. Between-group comparisons showed that, relative to HCs, HFS showed a lower pain-intensity rating to another's pain. Experiment 2 demonstrated that HFS had reduced empathy towards others' pain as a result of facial mimicry disorder. Taken together, study 2 revealed that different levels of mimicry led to different levels of empathy, suggesting that emotional mimicry is one of the mechanisms underlying pain empathy.
To investigate how empathy modulators affect empathy, in study 3, we compared event-related potentials (ERPs) in response to empathy-eliciting visual stimuli with a 2 (condition: pain vs. no-pain) × 3 (stimulus category: facial expressions, face pictures, and arm pictures) within-subject design. Pictures of painful expressions and needle-penetrated arms were treated as true-pain stimuli, while pictures of needle-penetrated faces with neutral expressions were considered false-pain as these situations were not commonly seen in daily life. The results revealed that, observers allocated more attentional resources to painful events compared to neutral ones, manifested as a positive shift in N2 and P3 components, when true-pain stimuli but not false-pain stimuli were presented. Therefore, the complex of N2 and P3 components may serve as a screening mechanism in brain through which observers bias their attentions towards more important or more relevant events in surroundings.
Taken together, the present study verified that pain empathy was accompanied by emotional mimicry, which had an causal role in empathic responses. People holds an attentional screening ability to automatically distinguish pain cues in the environment, which may lead to empathy difference towards different targets. We also discussed these phenomenon in an integrated theoretical perspective, i.e., 'simulation theory'.