Altered pain threshold sensitivity and frontoparietal-cingulate network in anorexia nervosa: the role of disgust sensitivity.

Abstract

The July issue included an interesting study1 investigating the contribution of the cingulate cortex in altered pain processing in anorexia nervosa. In particular, the study provides the first direct evidence of structural alterations (i.e., decreased grey matter volume and cortical thickness) in correspondence of the frontoparietal–cingulate network of this clinical population, which relates with their higher mean thermal pain threshold as well as with symptom severity and illness duration. According to these results, the authors conclude by arguing the existence of a common neural origin for thermal thresholds alterations and the clinical characteristics of anorexia nervosa. The neural and behavioural patterns reported by the authors suggest another, not mutually exclusive, interpretation of this result, which fits with the hypothesis of an altered disgust sensitivity in anorexia nervosa. First, we know that anorexia nervosa is affected by a consistently high disgust sensitivity.2 We also know that the experience of disgust and pain share common neural patterns of activity in the anterior, mid and posterior cingulate cortex and right parietal operculum.3 There is also evidence of a common autonomic nervous system activity in correspondence of the parasympathetic branch for both the experiences of pain4 and disgust.5 Finally, the recent study by Oaten and colleagues6 demonstrates that the experience of disgust is unique in generating a significant, increasing trend in pain sensitivity. For all these reasons, the absence of measures for assessing the subjective disgust sensitivity threshold in the anorexia nervosa participants represents an important limitation for interpreting the results reported by Bar and colleagues.1