Even though it is already known that anorexia nervosa comes with comparatively mild cognitive impairments, it is still unclear which neurobiological processes underlie them and how they develop in the course of the disease. This particularly counts for the influence of processing emotions, e.g. anxiety, though in this case the basic significance for the pathophysiology and course of anorexia nervosa is a matter of increasing discussion in literature. Consequently, we examined 22 female adolescent patients with AN both, during the period of starvation and shortly after short-term weight recovery by means of fMRT. 27 healthy persons served as control group. In the course of fMRT-examination Hariri’s paradigm about the comparison of faces of persons with different emotions was used. After weight recovery patients with AN compared with patients in the period of starvation selectively displayed a significantly increased neuronal activation in the somatomotor cortex when being shown anxious faces. In contrast to that no differences could be noticed cross-sectionally or longitudinally with neutral, angry, or surprised faces in comparison to healthy control persons. The longitudinal changes inactivation correlated with a lower BMI-SDS and a higher disease burden. The position in the somatosensoric cortex might indicate preparations or conditioning towards motoric actions in terms of a “fight or flight” reaction. The fact that the activity happens in the context of weight recovery might either indicate normalization of previous reduction in the period of starvation or a generally slightly increased reaction to anxiety with these patients at normal weight. Returning to enhanced anxiety reaction with increase in weight might be seen as a maintaining factor in AN. Enhanced levels of anxiety could also be seen within clinical variables, which highlights the possible relevance of these findings on a behavioral level. As the neurobiological changes mainly appear with anxiety and additionally are associated with serious diseases, this result brings anxiety even more into focus in the aetiology of the disease and additionally possibly as a maintaining factor. Consequently, this not only offers a base for futurere search in the underlying cerebral pathophysiology but also for studies in interventions which aim at the reduction of anxiety as the therapeutic objective.
Lukas Stanetzky (Wed,) studied this question.