This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. A high percentage of patients with an eating disorder (ED) diagnosis of anorexia or bulimia nervosa do not respond to current treatments of choice. This group of patients is more prone to drop out, use more clinical resources, and follow a chronic evolution of the disorder including death. The effects are devastating to patients and families and involve a high cost to society. Research into mechanisms that may explain the etiology and maintenance of persistent ED psychopathology is of great importance in order to improve its diagnosis, treatment and ultimately prevention. Binge eating is the most common behavior across ED diagnostic categories. The salient feature of a binge is loss of control over the eating episode. A predictor of poorer treatment response in individuals with EDs who binge-eat is high dietary restraint plus high negative affect. The combination of these two is related to lower impulse control, greater eating and comorbid psychopathology. Conversely, sustained recovery or early improvement from therapy seems related to a pure dietary subtype with individuals who are more able to control their impulses. However, a rigid pattern of dietary control may also lead to severe weight loss as in acute anorexia nervosa. Neural systems involved in flexible cognitive control of emotions and behaviors are located in the brain prefrontal cortex. However, an efficient functioning of this system is mediated by the striatum. To our knowledge, there are no studies on the direct contribution of cortico-striatal functioning to the etiology and maintenance of eating disorders, though a recent review of clinical, behavioral and neuroimaging studies shows indirect evidence of impairment in eating disordered individuals. Therefore, the aim of the present study is to map the activity of the cortico-striatal circuit in volunteered patients with EDs and compare it with data gathered from healthy adults during performance of a cognitive task of response anticipation designed to tap this neural network in a functional Magnetic Resonance Imaging (fMRI) experiment. Hypotheses: 1. When presented with ready versus relax cue condition in the task, ED patients will exhibit greater caudate and putamen activation (striatum) than controls. 2. When presented with incongruent versus congruent target conditions in the ready trials of the response anticipation task, ED patients will exhibit greater inefficiency in their ability to voluntary suppress the conflict as evidenced by less LPFC activation and greater ACC activation. 3. Greater striatal and ACC activity will correlate with greater ED symptomatology, negative affect and with lower impulse control. 4. ED patients will perform less accurately and rapidly in the target conditions of the response anticipation task than controls.
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