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Updated: May 21, 2026

Control of Eating Behavior Using a Novel Feedback System
Published on: May 8, 2018
Cognitive flexibility in juvenile anorexia nervosa patients before and after weight recovery
Katharina Bühren1, Verena Mainz, Beate Herpertz-Dahlmann
1Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital of the RWTH Aachen, Neuenhofer Weg 21, 52074 Aachen, Germany. kbuehren@ukaachen.de
Abstract:
Deficits in set-shifting abilities have been robustly described in adult patients with anorexia nervosa (AN). These deficits are associated with behavioral traits, such as rigidity and perfectionism, and are independent of starvation. However, little is known about neurocognitive deficits in juvenile patients with AN. The brain circuits that support set shifting are not fully mature in these patients. One possibility is that neuroendocrinological changes, such as elevated cortisol levels, contributing to alterations in cognitive performance in individuals with AN. Set-shifting abilities (Visual Set-Shifting Task), cortisol levels, self-reported perfectionism and obsessive personality traits were assessed in 28 female adolescent patients with AN before (T0) and after (T1) weight rehabilitation and compared with 27 age- and IQ-matched healthy controls (CG). Compared with the CG, AN patients showed increased reaction times (RT) in shift trials (p < 0.001) and reduced error rates in both shift and non-shift trials across time points (p < 0.05). Across all subjects, perfectionism was associated with increased RTs during shift trials at T1 (r = 0.35, p < 0.05). Subjects with lower cortisol levels showed increased RTs and more errors in non-shift trials (p < 0.05). In contrast to the findings in adult patients, adolescent patients with AN did not display a marked deficit in set-shifting abilities. Instead, they demonstrated a perfectionistic cognitive style that was characterized by increased RTs in shift trials but improved accuracy. One could speculate that the shorter duration of illness and the incomplete maturation of the prefrontal cortices contribute to these findings.
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