New study unravels neural mechanisms underlying inability to express emotions

This German study demonstrates that the supragenual anterior cingulate cortex (ACC) is constantly activated more strongly in alexithymic subjects and that this activation is related to the symptoms of alexithymia and not to associated symptoms such as depression. These findings also support the hypothesis of an altered function of the ACC in alexithymia.

A group of researchers of the University of Dusseldorf has performed a new study that unravels the neural mechanisms underlying the inability to express emotions (alexithymia). The findings are presented in the last 2010 issue of Psychotherapy and Psychosomatics.

One of the most prominent neurobiological models of alexithymia assumes an altered function of the anterior cingulate cortex (ACC) as the crucial neural correlate of alexithymia. So far functional imaging studies have yielded inconclusive results. A group of German researchers tested this hypothesis in healthy alexithymics and nonalexithymics in an event-related fMRI study.

Thirty high- and 30 low-alexithymic right-handed male subjects (selected by the 20-item Toronto Alexithymia Scale, TAS-20) were investigated with event-related fMRI using a picture viewing paradigm. The stimuli consisted of happy, fearful and neutral facial expressions (Ekman-Friesen) as well as positive, negative and neutral pictures from the International Affective Picture System.

Contrasting the high-alexithymic with the low-alexithymic group the researchers observed increased activation of the supragenual ACC for different emotional valences as well as for different emotional stimuli. Moreover, there was a positive correlation of the ACC with the individual TAS-20 scores but no correlations with the individual Beck Depression Inventory scores. Additionally, there was no difference in activity of the amygdala.

This study demonstrated that the supragenual ACC is constantly activated more strongly in alexithymic subjects and that this activation is related to the symptoms of alexithymia and not to associated symptoms such as depression. Therefore, these findings support the hypothesis of an altered function of the ACC in alexithymia.