This article argues that mirror neurons originate in sensorimotor associative learning and therefore a new approach is needed to investigate their functions. Mirror neurons were discovered about 20 years ago in the monkey brain, and there is now evidence that they are also present in the human brain. The intriguing feature of many mirror neurons is that they fire not only when the animal is performing an action, such as grasping an object using a power grip, but also when the (...) animal passively observes a similar action performed by another agent. It is widely believed that mirror neurons are a genetic adaptation for action understanding; that they were designed by evolution to fulfill a specific socio-cognitive function. In contrast, we argue that mirror neurons are forged by domain-general processes of associative learning in the course of individual development, and, although they may have psychological functions, they do not necessarily have a specific evolutionary purpose or adaptive function. The evidence supporting this view shows that mirror neurons do not consistently encode action “goals”; the contingency- and context-sensitive nature of associative learning explains the full range of mirror neuron properties; human infants receive enough sensorimotor experience to support associative learning of mirror neurons ; and mirror neurons can be changed in radical ways by sensorimotor training. The associative account implies that reliable information about the function of mirror neurons can be obtained only by research based on developmental history, system-level theory, and careful experimentation. (shrink)
Alexithymia is characterized by difficulty identifying and describing one’s own emotion. Identifying and describing one’s emotion involves several cognitive processes, so alexithymia may result from a number of impairments. Here we propose the alexithymia language hypothesis—the hypothesis that language impairment can give rise to alexithymia—and critically review relevant evidence from healthy populations, developmental disorders, adult-onset illness, and acquired brain injury. We conclude that the available evidence is supportive of the alexithymia–language hypothesis, and therefore that language impairment may represent one of (...) multiple routes to alexithymia. Where evidence is lacking, we outline which approaches will be useful in testing this hypothesis. (shrink)
Commentators have tended to focus on the conceptual framework of our article, the contrast between genetic and associative accounts of mirror neurons, and to challenge it with additional possibilities rather than empirical data. This makes the empirically focused comments especially valuable. The mirror neuron debate is replete with ideas; what it needs now are system-level theories and careful experiments – tests and testability.