Reward processing in anorexia nervosa

Monash Alfred Psychiatry Research Centre, Monash University, Central Clinical School, The Alfred, Australia.
Neuropsychologia (Impact Factor: 3.3). 02/2012; 50(5):567-75. DOI: 10.1016/j.neuropsychologia.2012.01.036
Source: PubMed

ABSTRACT Individuals with anorexia nervosa (AN) demonstrate a relentless engagement in behaviors aimed to reduce their weight, which leads to severe underweight status, and occasionally death. Neurobiological abnormalities, as a consequence of starvation are controversial: evidence, however, demonstrates abnormalities in the reward system of patients, and recovered individuals. Despite this, a unifying explanation for reward abnormalities observed in AN and their relevance to symptoms of the illness, remains incompletely understood. Theories explaining reward dysfunction have conventionally focused on anhedonia, describing that patients have an impaired ability to experience reward or pleasure. We review taste reward literature and propose that patients' reduced responses to conventional taste-reward tasks may reflect a fear of weight gain associated with the caloric nature of the tasks, rather than an impaired ability to experience reward. Consistent with this, we propose that patients are capable of 'liking' hedonic taste stimuli (e.g., identifying them), however, they do not 'want' or feel motivated for the stimuli in the same way that healthy controls report. Recent brain imaging data on more complex reward processing tasks provide insights into fronto-striatal neural circuit dysfunction related to altered reward processing in AN that challenges the relevance of anhedonia in explaining reward dysfunction in AN. In this way, altered activity of the anterior cingulate cortex and striatum could explain patients' pathological engagement in behaviors they consider rewarding (e.g., self-starvation) that are otherwise aversive or punishing, to those without the eating disorder. Such evidence for altered patterns of brain activity associated with reward processing tasks in patients and recovered individuals may provide important information about mechanisms underlying symptoms of AN, their future investigation, and the development of treatment approaches.

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Available from: Susan L Rossell, Sep 25, 2015
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    • "Though we can only provide a brief discussion of three such disorders here, the potential exists for many others . For instance, Obsessive-Compulsive disorder, where behavior may exhibit an overreliance on habits due to dysfunctional goaldirected circuitry (Gillan et al., 2011), and anorexia nervosa, where there is a tendency to deprive oneself of food, despite, or likely because of, hyperactivity in evaluative neural circuitry during food presentation (Keating et al., 2012), provide interesting examples. "
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    ABSTRACT: The ability to learn contingencies between actions and outcomes in a dynamic environment is critical for flexible, adaptive behavior. Goal-directed actions adapt to changes in action-outcome contingencies as well as to changes in the reward-value of the outcome. When networks involved in reward processing and contingency learning are maladaptive, this fundamental ability can be lost, with detrimental consequences for decision-making. Impaired decision-making is a core feature in a number of psychiatric disorders, ranging from depression to schizophrenia. The argument can be developed, therefore, that seemingly disparate symptoms across psychiatric disorders can be explained by dysfunction within common decision-making circuitry. From this perspective, gaining a better understanding of the neural processes involved in goal-directed action, will allow a comparison of deficits observed across traditional diagnostic boundaries within a unified theoretical framework. This review describes the key processes and neural circuits involved in goal-directed decision-making using evidence from animal studies and human neuroimaging. Select studies are discussed to outline what we currently know about causal judgments regarding actions and their consequences, action-related reward evaluation, and, most importantly, how these processes are integrated in goal-directed learning and performance. Finally, we look at how adaptive decision-making is impaired across a range of psychiatric disorders and how deepening our understanding of this circuitry may offer insights into phenotypes and more targeted interventions.
    Frontiers in Systems Neuroscience 05/2014; 8:101. DOI:10.3389/fnsys.2014.00101
    • "starvation) become reinforced. Recent evidence suggests that dysfunctional reward-processing may even be a biological marker for anorexia nervosa (Keating et al., 2012). Individuals with anorexia nervosa also display cognitive deficits that may be related to disrupted decision-making, such as poor attentional control, memory impairments, and disrupted executive functioning (see Lena, Fiocco, & Leyenarr (2004) for a review; Wilsdon & Wade, 2006). "
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    ABSTRACT: Discounting tasks are ideal paradigms for examining impulsivity in decision-making processes. Eating disorders, such as anorexia nervosa, are associated with increased impulsivity, poor coping, and dysfunctional reward-processing, all of which have implications for how these individuals manage decisions, both in and out of treatment. The current study examined discounting behavior in women at risk for anorexia nervosa as a novel way to examine decision-making processes within this population. Results suggest that women at risk for anorexia nervosa display increased impulsivity in certain decision-making contexts. These results have implications for the conceptualization and treatment of women with or at-risk for disordered eating.
    07/2013; 1(2):148-160. DOI:10.1080/21662630.2013.794514
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    • "Our findings primarily highlight the mPFC, which is widely implicated in a number of fundamental cognitive processes related to affect regulation (Ochsner and Gross, 2005; Etkin et al., 2006), value-based decision-making (Rushworth et al., 2004; Wallis and Kennerley, 2010), and self-evaluation and negative self-judgment (Enzi et al., 2009). Importantly, structural, functional, and neurochemical alterations in mPFC have been reported across a number of psychiatric diagnoses (Coryell et al., 2005; Fitzgerald et al., 2008; Goldstein et al., 2009; Koch et al., 2009; Shin et al., 2009; Fineberg et al., 2010; Treadway and Zald, 2011; Gabbay et al., 2012; Keating et al., 2012). Taken together these findings implicate mPFC as a transdiagnostic nexus, wherein dysfunction predisposes diverse forms of psychopathology that, while categorically distinct, may be symptomatically related due to shared deficits in mPFCsubserved cognitive processes (Buckholtz and Meyer-Lindenberg, 2012). "
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    ABSTRACT: Stress is a significant risk factor for the development of psychopathology, particularly symptoms related to reward processing. Importantly, individuals display marked variation in how they perceive and cope with stressful events, and such differences are strongly linked to risk for developing psychiatric symptoms following stress exposure. However, many questions remain regarding the neural architecture that underlies inter-subject variability in perceptions of stressors. Using functional magnetic resonance imaging (fMRI) during a Monetary Incentive Delay (MID) paradigm, we examined the effects of self-reported perceived stress levels on neural activity during reward anticipation and feedback in a sample of healthy individuals. We found that subjects reporting more uncontrollable and overwhelming stressors displayed blunted neural responses in medial prefrontal cortex (mPFC) following feedback related to monetary gains as well monetary losses. This is consistent with preclinical models that implicate the mPFC as a key site of vulnerability to the noxious effects of uncontrollable stressors. Our data help translate these findings to humans, and elucidate some of the neural mechanisms that may underlie stress-linked risk for developing reward-related psychiatric symptoms.
    Frontiers in Human Neuroscience 05/2013; 7:180. DOI:10.3389/fnhum.2013.00180 · 2.99 Impact Factor
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