Reply: Spontaneous versus deliberate vicarious representations: different routes to empathy in psychopathy and autism.

Sir, We thank Gillespie et al. (2014) for their letter. They summarize data that suggest that in autism, vicarious activations can be relatively normal under instructions explicitly encouraging vicarious processes, while being abnormal in conditions in which instructions do not. This points to an important opportunity to improve our understanding of empathy—both with regards to deficits in patients and individual differences in the normal population. To date, the ‘cake’ called empathy has been cut in various ways. Some cut it in two pieces, cognitive versus emotional empathy (Baron-Cohen and Wheelwright, 2004), acknowledging that somewhat separate systems support the capacity to think what another is thinking (cognitive empathy) and to feel what another is feeling (emotional empathy). This has influenced our thinking about individual variability in empathy and psychiatric disorders, with some disorders, like autism, thought to be impaired more in cognitive empathy whereas others, like psychopathy, are impaired more in emotional empathy (Blair, 2005). Based on neuroscience, we have ‘cut’ empathy into four pieces: motor, emotional, tactile and cognitive empathy (Keysers and Gazzola, 2009). Mirror neurons in motor cortices and functional MRI activations in motor cortices during action observation suggest motor empathy: vicariously activating one’s own actions while witnessing the actions of others (Gallese et al., 1996; Gazzola and Keysers, 2009; Keysers, 2009; Caspers et al., 2010). Later, neuroimaging data showed that one also vicariously activate neural substrates involved in one’s own disgust (Wicker et al., 2003) and pain (Lamm et al., 2011) while witnessing the disgust or pain of others, suggesting emotional empathy. Somatosensory brain regions were also found to be vicariously active when viewing the tactile and haptic sensations of others, suggesting somatosensory empathy (Keysers et al., 2004, 2010; Gazzola and Keysers, 2009; Caspers et al., 2010). Finally, reasoning about the beliefs of others vicariously activates ventral medial prefrontal regions involved in reasoning about one’s own beliefs, suggesting cognitive empathy (Mitchell et al., 2006). Because these forms of empathy recruit partially distinct neural substrates, and specific lesions can impair specific domains of empathy (Calder et al., 2000; Pazzaglia et al., 2008), neuroscientific data suggest that empathy is indeed composed of partly separated modalities. What our data (Meffert et al., 2013), and those reviewed by Gillespie et al. (2014), suggest is that the cake of empathy can be cut in another, psychiatrically and neurologically relevant, direction as well: not by domain (motor, emotional, somatosensory or cognitive) but by how deliberately one empathizes. In our psychopathic individuals, we found that spontaneous motor, somatosensory and emotional empathy is reduced while their deliberate counterparts are not (Meffert et al., 2013). The data reviewed by Gillespie et al. (2014) suggest that in autism, deliberate motor empathy might be intact, whereas spontaneous motor empathy might not be. In addition, neurological data suggest, that after lesions to the amygdala, spontaneous emotion processing is compromised, whereas deliberate processing under instructions to look at eye regions might be preserved (Adolphs et al., 2005). From a neurological or psychiatric point of view, the question is then no longer: ‘is that patient’s empathy intact or not?’, instead, one would need to check the four modalities of empathy separately, and entertain the possibility, that for each of these, deliberate and spontaneous empathy might not necessarily be equally functional (Fig. 1). This distinction of deliberate versus spontaneous should not be confused with the cognitive versus affective doi:10.1093/brain/awt376 Brain 2014: 137; 1–4 | e273