OBJECTIVE: It is well known that individuals with anorexia nervosa (AN) are inhibited and over-controlled. This study investigated a prefrontal-cingulate network that is involved in inhibitory control. METHOD: To avoid the confounds of malnutrition, 12 recovered (RAN) subjects were compared to 12 matched control women (CW) using a validated inhibition task (i.e., a stop signal task) during functional magnetic resonance imaging. RESULTS: Consistent with the a priori hypothesis, RAN subjects showed altered task-related activation in the medial prefrontal cortex (mPFC), a critical node of the inhibitory control network. Specifically, whereas RAN and CW showed similar mPFC activity during trials when inhibitory demand was low (i.e., easy trials), RAN relative to CW showed significantly less mPFC activation as inhibition trials became more difficult (i.e., hard trials), suggesting a demand-specific modulation of inhibitory control circuitry in RAN. DISCUSSION: These findings support a neural basis for altered impulse control symptoms in AN.
OBJECTIVE: It is well known that individuals with anorexia nervosa (AN) are inhibited and over-controlled. This study investigated a prefrontal-cingulate network that is involved in inhibitory control. METHOD: To avoid the confounds of malnutrition, 12 recovered (RAN) subjects were compared to 12 matched control women (CW) using a validated inhibition task (i.e., a stop signal task) during functional magnetic resonance imaging. RESULTS: Consistent with the a priori hypothesis, RAN subjects showed altered task-related activation in the medial prefrontal cortex (mPFC), a critical node of the inhibitory control network. Specifically, whereas RAN and CW showed similar mPFC activity during trials when inhibitory demand was low (i.e., easy trials), RAN relative to CW showed significantly less mPFC activation as inhibition trials became more difficult (i.e., hard trials), suggesting a demand-specific modulation of inhibitory control circuitry in RAN. DISCUSSION: These findings support a neural basis for altered impulse control symptoms in AN.
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