The present study employs a new framework to categorise the heterogeneous findings on the relationship between impaired reward processing and negative and affective symptoms of schizophrenia. Based on previous behavioural and neuroimaging studies we postulate that "wanting" (i.e. anticipation) of a reward is specifically related to apathy, whereas "liking" (i.e. hedonic impact) is related to anhedonia and depression-symptoms commonly observed in schizophrenia. Fifteen patients with schizophrenia or schizoaffective disorder treated with atypical antipsychotic drugs and fifteen healthy controls performed a probabilistic monetary incentive delay task while undergoing functional magnetic resonance imaging. At the group level we found no significant differences between patients and controls in neural activation during anticipation or receipt of a reward. However, in patients with schizophrenia specific relationships between ventral-striatal activation and symptoms were observed. Ventral-striatal activation during reward anticipation was negatively correlated with apathy, while activation during receipt of reward was negatively correlated with severity of depressive symptoms. These results suggest that the link between negative symptoms and reward anticipation might specifically relate to apathy, i.e. a lack of motivation and drive. Impaired hedonic reward processing might contribute to the development of depressive symptoms in patients with schizophrenia, but it is not directly associated with self-rated anhedonia. These results indicate the necessity of more specifically differentiating negative and affective symptoms in schizophrenia in order to understand the role of the reward system in their pathogenesis.

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Recent models of the development of addiction propose a transition from a pleasure-driven to a heavily automatized behaviour, marked by a loss of cognitive control. This study investigated the deficits in different components of cognitive functions including behavioural inhibition in response to alcohol-related stimuli in alcohol-dependent patients (ADP) and healthy controls (HC). The aims of the study were to identify which particular cognitive functions are impaired in ADP. Furthermore, we analysed the association between cognitive deficits and relapse rates and the reversibility of cognitive deficits under abstinence in a 6-month follow-up period. Ninety-four recently detoxified ADP and 71 HC completed the cognitive tasks as well as questionnaire measures assessing drinking behaviour and personality traits. Compared with HC, ADP showed poorer performance in response initiation, response inhibition, complex-sustained attention and executive functions. Impairment in response inhibition was a significant predictor for relapse, yet the strongest predictor was the interaction between the number of previous detoxifications and response-inhibition deficits. The results of a moderation analysis showed that patients with many previous detoxifications and large deficits in response inhibition showed the highest relapse risk. These findings indicate that interventions should take into account inhibitory deficits especially in ADP with a high number of previous detoxifications.

Clinical observations and similarities to addiction suggest heightened reward sensitivity to food in patients with bulimictype eating (BTE) disorders. Therefore, we investigated the expectation and receipt of food reward compared with monetary reward in patients with BTE. Fifty-six patients with BTE (27 patients with binge eating disorder and 29 with bulimia nervosa) and 55 matched healthy control participants underwent event-related functional magnetic resonance imaging while performing both food and monetary incentive delay tasks. BTE patients exhibited reduced brain activation in the posterior cingulate cortex during the expectation of food and increased activity in the medial orbitofrontal cortex, anterior medial prefrontal cortex and posterior cingulate cortex during the receipt of food reward. These findings were relevant to food because we found no significant group differences related to monetary reward. In the patients, higher brain activity in the medial orbitofrontal cortex during the receipt of food reward was related to higher levels of trait food craving and external eating. BTE patients exhibited increased hedonic processing during the receipt of food reward. These findings corroborate the notion that an altered responsiveness of the reward network to food stimuli is associated with BTE.