An fMRI Study of Self-Regulatory Control and Conflict Resolution in Adolescents With Bulimia Nervosa

Abstract

Objective The authors examined functional activity in the frontostriatal systems that mediate self-regulatory capacities and conflict resolution in adolescents with bulimia nervosa. Method Functional magnetic resonance imaging was used to compare blood-oxygen-level-dependent response in 18 female adolescents with bulimia nervosa and 18 healthy female age-matched subjects during performance on a Simon spatial incompatibility task. Bayesian analyses were used to compare the two groups on patterns of brain activation during correct responses to conflict stimuli and to explore the effects of antecedent stimulus context on group differences in self-regulation and conflict resolution. Results Adolescents with and without bulimia nervosa performed similarly on the task. During correct responses in conflict trials, frontostriatal circuits—including the right inferolateral and dorsolateral prefrontal cortices and putamen—failed to activate to the same degree in adolescents with bulimia nervosa as in healthy comparison subjects. Instead, deactivation was seen in the left inferior frontal gyrus as well as a neural system encompassing the posterior cingulate cortex and superior frontal gyrus. Group differences in cortical and striatal regions were driven by the differential responses to stimuli preceded by conflict and nonconflict stimuli, respectively. Conclusions When engaging the self-regulatory control processes necessary to resolve conflict, adolescents with bulimia nervosa displayed abnormal patterns of activation in frontostriatal and default-mode systems. Their abnormal processing of the antecedent stimulus context conditioned their brain response to conflict differently from that of healthy comparison subjects, specifically in frontal regions. It is suspected that functional disturbances in frontal portions of frontostriatal systems may release feeding behaviors from regulatory control, thereby perpetuating the conflicting desires to consume fattening foods and avoid weight gain that characterize bulimia nervosa.

Neural signature of behavioural inhibition in women with bulimia nervosa

“…26 However, 2 previous studies addressing general cognitive inhibition in adolescents and adults support diminished activity in the frontostriatal network during inhibitory control. 27,28 In the present study, significant differences within frontostriatal networks were observed only in patients with bulimia nervosa with 3 or more binge eating/purging episodes per week. Patients with less severe symptoms showed no significant neural alterations compared with healthy controls and patients with high symptom severity.…”

“…Previous studies investigating cognitive inhibition 27,28 have identified diminished activation of the right lateral PFC and striatum as core regions of impaired inhibitory control in patients with bulimia nervosa. A meta-analysis 48 has identified clusters of activation in the PFC, pre-SMA and insula during behavioural inhibition.…”

“…Adolescent patients with bulimia nervosa with the most objective bulimic and vomiting episodes deactivated the inferior frontal gyrus and precuneus. 27 Adults with the disorder with the most objective episodes of binge eating/purging engaged cortical areas (medial PFC, TC, inferior parietal cortex) and the head of the caudate nucleus the least. 28 These results suggest that the association of cortical-subcortical activation with symptom severity is dose-dependent.…”

“…However, a limitation of this study was that the authors grouped anorexia nervosa from the binge eating/purging subtype together with bulimia nervosa in a single category of binge eating/purging behaviour, limiting the specificity of the results to either the binge eating/purging subtype of anorexia nervosa or bulimia nervosa. Furthermore, neural correlates of cognitive inhibition (i.e., interference control) have been assessed in adolescents 27 and adults 28 with bulimia nervosa. During correct responding on incongruent nonfood trials, adolescent and adult patients showed diminished activation in frontostriatal circuits, including the right lateral PFC and striatum.…”

Neural Dysfunction in Cognitive Control Circuits in Persons at Clinical High-Risk for Psychosis

“…This probability is displayed in a Posterior Probability Map. Because the Bayesian method infers posterior probability, by definition, it does not generate false positives and therefore does not require adjustment of its p-values based on p-value thresholding, as shown previously (Friston and Penny, 2003;Marsh et al, 2011). We adopted a similar approach as in Klein et al (2007) but with a more stringent threshold.…”