Deficient Activity in the Neural Systems That Mediate Self-regulatory Control in Bulimia Nervosa

Department of Psychiatry, New York State Psychiatric Institute and the College of Physicians and Surgeons, Columbia University, New York, New York.
Archives of general psychiatry (Impact Factor: 14.48). 02/2009; 66(1):51-63. DOI: 10.1001/archgenpsychiatry.2008.504
Source: PubMed

ABSTRACT Disturbances in neural systems that mediate voluntary self-regulatory processes may contribute to bulimia nervosa (BN) by releasing feeding behaviors from regulatory control.
To study the functional activity in neural circuits that subserve self-regulatory control in women with BN.
We compared functional magnetic resonance imaging blood oxygenation level-dependent responses in patients with BN with healthy controls during performance of the Simon Spatial Incompatibility task.
University research institute.
Forty women: 20 patients with BN and 20 healthy control participants. Main Outcome Measure We used general linear modeling of Simon Spatial Incompatibility task-related activations to compare groups on their patterns of brain activation associated with the successful or unsuccessful engagement of self-regulatory control.
Patients with BN responded more impulsively and made more errors on the task than did healthy controls; patients with the most severe symptoms made the most errors. During correct responding on incongruent trials, patients failed to activate frontostriatal circuits to the same degree as healthy controls in the left inferolateral prefrontal cortex (Brodmann area [BA] 45), bilateral inferior frontal gyrus (BA 44), lenticular and caudate nuclei, and anterior cingulate cortex (BA 24/32). Patients activated the dorsal anterior cingulate cortex (BA 32) more when making errors than when responding correctly. In contrast, healthy participants activated the anterior cingulate cortex more during correct than incorrect responses, and they activated the striatum more when responding incorrectly, likely reflecting an automatic response tendency that, in the absence of concomitant anterior cingulate cortex activity, produced incorrect responses.
Self-regulatory processes are impaired in women with BN, likely because of their failure to engage frontostriatal circuits appropriately. These findings enhance our understanding of the pathogenesis of BN by pointing to functional abnormalities within a neural system that subserves self-regulatory control, which may contribute to binge eating and other impulsive behaviors in women with BN.

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Available from: Rachel Marsh, Sep 29, 2015
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    • "We add that careful attention to differences associated with task parameters and sampling characteristics is warranted when attempting to interpret results obtained across studies in the ED literature. In this literature, some studies applying tasks presumed to tap frontal inhibitory controls show relatively weaker activations in frontal regions when comparing individuals displaying bulimic symptomatology to healthy control groups (Marsh et al., 2009; Joos et al., 2011), whereas others show relatively stronger activations (e.g., Lock et al, 2011). We suspect that apparent discrepancies may reflect differential brain-activation patterns associated with such factors as age, illness chronicity, comorbid traits, and variable task demands. "
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    Psychiatry Research: Neuroimaging 02/2015; 232(1). DOI:10.1016/j.pscychresns.2015.01.022 · 2.42 Impact Factor
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    • "Consequently, an alteration in the function of this brain area would be expected to result in aberrant food intake and the development of feeding related pathologies. Indeed, functional magnetic resonance imaging (fMRI) of people exhibiting diseases of disordered feeding such as bulimia often show activity changes in prefrontal cortex such as in Brodmann’s area 32 (Marsh et al., 2009; Lock et al., 2011). Interestingly, anorexics and obese individuals show opposite changes in PFC activity as measured by fMRI in a taste reward task when compared to controls (Frank et al., 2012), suggesting that altered PFC function may be driving the observed pathological changes in feeding behavior. "
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    • "circuits to the same degree as healthy controls (Marsh et al., 2009). Clinically, patients with anorexia nervosa display a remarkable ability to control their food intake behavior (Mayer et al., 2012) and demonstrate enhanced ability to delay monetary (e.g. "
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