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Updated: Apr 18, 2026

Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa
Published on: October 22, 2015
Implicit sequence learning in juvenile anorexia nervosa: neural mechanisms and the impact of starvation
Christine Firk1, Verena Mainz1, Martin Schulte-Ruether1,2
1Department of Child and Adolescent Psychiatry, University Hospital RWTH Aachen, Aachen, Germany.
Background:
Previous studies have reported that cognitive deficits occur in patients with anorexia nervosa (AN) and that these deficits may represent a predisposition towards developing AN or perpetuate the disorder. Specifically, dysfunctional implicit learning may contribute to the development of highly resistant dieting behaviours that are fundamental to the persistence of the disorder. Thus, the aims of this study were (a) to investigate implicit sequence learning in adolescent patients with AN before and after weight recovery and (b) to elucidate the associated neural mechanisms in acute AN relative to healthy controls.
Methods:
In a behavioural study, implicit sequence learning was assessed using a serial reaction time task in 27 adolescents with AN before (T1) and after weight recovery (T2) compared with age-matched healthy controls (HC) who were assessed at similar time intervals. The neural correlates of implicit sequence learning were subsequently investigated in 19 AN patients shortly after they were admitted to the hospital and 20 HC using functional magnetic resonance imaging (fMRI).
Results:
At T1, AN patients showed reduced sequence learning compared with HC. However, no behavioural differences between HC and AN patients were found at T2. At the neural level, acute AN patients showed reduced thalamic activation during sequence learning compared with HC subjects.
Conclusions:
Our data suggest that the impaired implicit learning observed in adolescent AN patients before weight gain is a state-related dysfunction that normalises with weight gain. Thus, implicit learning deficits do not appear to represent a predisposition towards developing AN; rather, these deficits should be considered when planning psychotherapeutic interventions for acute AN. Reduced thalamic activation during the acute stage of AN may indicate a starvation-induced dysfunction of the neural circuitry that is involved in behavioural flexibility.
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