Altered cortical thickness and attentional deficits in adolescent girls and women with bulimia nervosa

Abstract

Background: Frontostriatal and frontoparietal abnormalities likely contribute to deficits in control and attentional processes in individuals with bulimia nervosa and to the persistence of dysregulated eating across development. This study assessed these processes and cortical thickness in a large sample of adolescent girls and women with bulimia nervosa compared with healthy controls.

Methods: We collected anatomical MRI data from adolescent girls and women (ages 12-38 yr) with full or subthreshold bulimia nervosa and age-matched healthy controls who also completed the Conners Continuous Performance Test-II (CPT-II). Groups were compared on task performance and cortical thickness. Mediation analyses explored associations among cortical thickness, CPT-II variables, bulimia nervosa symptoms and age.

Results: We included 60 girls and women with bulimia nervosa and 54 controls in the analyses. Compared with healthy participants, those with bulimia nervosa showed increased impulsivity and inattention on the CPT-II, along with reduced thickness of the right pars triangularis, right superior parietal and left dorsal posterior cingulate cortices. In the bulimia nervosa group, exploratory analyses revealed that binge eating frequency correlated inversely with cortical thickness of frontoparietal and insular regions and that reduced frontoparietal thickness mediated the association between age and increased symptom severity and inattention. Binge eating frequency also mediated the association between age and lower prefrontal cortical thickness.

Limitations: These findings are applicable to only girls and women with bulimia nervosa, and our cross-sectional design precludes understanding of whether cortical thickness alterations precede or result from bulimia nervosa symptoms.

Conclusion: Structural abnormalities in the frontoparietal and posterior cingulate regions comprising circuits that support control and attentional processes should be investigated as potential contributors to the maintenance of bulimia nervosa and useful targets for novel interventions.

Fig. 1

(A) Group differences in cortical thickness (p < 0.05, false discovery rate [FDR]–corrected). Cool colours (blues) indicate reduced thickness, and warm colours (reds) indicate greater thickness in the bulimia nervosa (BN) compared with the control group (HC). Analyses include age as a covariate. The colour bar indicates t values. Corresponding statistics are presented in Appendix 1, Table S2. (B) Group × age interaction effect on cortical thickness (p < 0.05, FDR-corrected). Cortical thickness of the right isthmus cingulate (Isth Cing) was inversely associated with age in the healthy control group and positively associated with age in the bulimia nervosa group, contributing to a group × age interaction. Corresponding statistics are presented in Appendix 1, Table S4. dPCC = dorsal posterior cingulate cortex; pars triang = pars triangularis; SPC = superior parietal cortex; vPCC = ventral posterior cingulate cortex.

Fig. 2

Associations of cortical thickness (CT) with loss of control eating episodes (LOCEs) in the bulimia nervosa group. Blue colours indicate inverse associations of cortical thickness with the frequency of binge-eating episodes before MRI scanning, with smaller p values in darker shades. (A) Cortical thickness, adjusted for age, is plotted on the Y axis, with log-transformed objective bulimic episodes (OBEs; previous 3 months) plotted on the X axis. All effect sizes for associations between cortical thickness and OBEs were medium. (B) Cortical thickness, adjusted for age, is plotted on the Y axis, with log-transformed LOCEs (previous month) plotted on the X axis. Three outliers in the distribution of LOCEs were detected (p = 0.012), but none were detected in the distribution of OBEs (p = 0.46). Studentized residuals of regression models confirmed that effects in the bilateral insula were not outlier-driven (left p = 0.50; right p = 0.69), but effects in the right insula became marginally significant (p = 0.08) after excluding 2 13-year-olds without LOCEs in the previous month. Ins = insula; IPC = inferior parietal cortex; rMFG = rostral middle frontal gyrus.

Fig. 3

Mediation models within the bulimia nervosa (BN) group. (A) Lower cortical thickness in the bilateral insula (yellow) mediated the association between advancing age and increased frequency of loss of control eating episodes (LOCEs; previous month). (B) More frequent objective bulimic episodes (OBEs; previous 3 months) mediated the association between age and lower cortical thickness in the left rostral middle frontal gyrus (rMFG; magenta). Indirect effects and 95% confidence intervals are shown below mediation models in panels A and B. (C) Lower thickness of bilateral pars opercularis (Pars Operc) and right pars triangularis (Pars Triang), inferior parietal cortex (IPC), and insula (Ins) mediated the association between age and Conners Continuous Performance Test-II (CPT-II) measures of inattention in the bulimia nervosa sample. Estimates and significance levels for each path in this model (model C in Appendix 1, Fig. S1) are presented in Appendix 1, Table S7.