Towards a neurobiological understanding of alexithymia.

Although the specialized literature on the etiology of alexithymia is controversial, neurobiological research has shown relevant advances. The aim of this review is to analyze the available evidence regarding the neurophysiological bases of alexithymia. A comprehensive review of available articles from Medline/PubMed, EBSCO and SciELO was conducted. Previously, alexithymia was linked to a reduced interhemispheric brain connection. From a childhood traumatic perspective, the right prefrontal cortex and the default mode network would experience alterations, first hypermetabolic (dopaminergic and glutamatergic dysregulation) and then hypometabolic-dissociative (serotonergic and opioid dysregulation), resulting in a distorted interoceptive and emotional awareness. Mirror neurons are the essential neurobiological substrate of theory of mind and social cognition, intrinsically linked to alexithymia, involving parietal, temporal, premotor, and cingulate cortices, and inferior frontal gyrus. Other structures involved are the amygdala (facial expression and emotional reactivity), the insula (interoception, emotional integration and empathy) and the cerebellum (limbic cerebellum and somatosensory awareness). Molecular genetics has detected polymorphisms in genes of the serotonin transporter, in the enzyme genes of dopaminergic metabolism and brain-derived neurotrophic factor, while the role of oxytocin is controversial. To sum up, we found several studies demonstrating the overwhelming evidence of a neurobiological basis underlying alexithymia; nevertheless, research is still inconclusive and must include environmental, traumatic, social, and psychological factors that contribute to the origin of the alexithymia.