No abstract

The spontaneous tendency to synchronize our facial expressions with those of others is often termed emotional contagion. It is unclear, however, whether emotional contagion depends on visual awareness of the eliciting stimulus and which processes underlie the unfolding of expressive reactions in the observer. It has been suggested either that emotional contagion is driven by motor imitation (i.e., mimicry), or that it is one observable aspect of the emotional state arising when we see the corresponding emotion in others. Emotional contagion reactions to different classes of consciously seen and ''unseen'' stimuli were compared by presenting pictures of facial or bodily expressions either to the intact or blind visual field of two patients with unilateral destruction of the visual cortex and ensuing phenomenal blindness. Facial reactions were recorded using electromyography, and arousal responses were measured with pupil dilatation. Passive exposure to unseen expressions evoked faster facial reactions and higher arousal compared with seen stimuli, therefore indicating that emotional contagion occurs also when the triggering stimulus cannot be consciously perceived because of cortical blindness. Furthermore, stimuli that are very different in their visual characteristics, such as facial and bodily gestures, induced highly similar expressive responses. This shows that the patients did not simply imitate the motor pattern observed in the stimuli, but resonated to their affective meaning. Emotional contagion thus represents an instance of truly affective reactions that may be mediated by visual pathways of old evolutionary origin bypassing cortical vision while still providing a cornerstone for emotion communication and affect sharing.affective blindsight ͉ electromyography ͉ emotional body language ͉ motor resonance ͉ emotional contagion ͉ face

Significant ALE values related to GM increases were observed bilaterally in the cerebellum, in the middle temporal gyrus, in the right anterior cingulate cortex, caudate head, insula, fusiform gyrus, precuneus and posterior cingulate cortex, and in the left lingual gyrus. GM decreases were observed bilaterally in the cerebellar tonsil and inferior parietal lobule, in the right amygdala, insula, middle temporal gyrus, caudate tail and precuneus and in the left precentral gyrus.