Too much, too little. Understanding the mechanisms underlying disorders of excessive and diminished motivation.

Motivation is a complex process essential for the survival of individuals that produces behaviors in response to the changing of internal and environmental conditions (Salamone et al., 2016; Simpson and Balsam, 2016). A key variable influencing motivation is the availability of rewards. Indeed, in everyday life, rewards motivate behavior and provide enjoyment, favoring adaptation and health functioning. However, motivated behavior can get disrupted, leading to different pathological misdirection of motivation including apathy, anhedonia and impulse control disorders (ICD). Therefore, the aim of the present thesis is to investigate processes, such as reward responsiveness (reward liking and wanting) and reward valuation (temporal and effort discounting of rewards), that have been considered as likely contributors of abnormal motivation across neurological and psychiatric disorders. All these aspects are introduced in Chapter 1 of my thesis, while in the following Chapters (2-3) I will report original studies in which I used different techniques to explore disorders of excessive (Chapter 2) and diminished (Chapter 3) motivation. In Study 1, reward responsiveness was investigated in Parkinson’s disease (PD) patients with binge eating (BE) by asking them to perform different experimental tasks assessing food liking and wanting (Chapter 2). The results of this study showed that BE in PD was associated with cognitive abnormalities, and to lesser extent affective abnormalities, but not with an increased wanting of rewards. In Study 2 I tested the hypothesis that PD patients with different impulse control disorders (ICD) may have altered reward responsiveness and reward valuation, and that the DLPFC may have a causal role in such alterations. In this study transcranial direct current stimulation (tDCS) over DLPFC was used when PD patients with and without ICD and healthy matched controls performed a reward responsiveness task employing explicit (self-ratings of liking and wanting) and implicit (heart beat and skin conductance response) measures, and two temporal discounting tasks in order to measure their reward valuation processes. Results showed that patients with ICD and PD have a greater liking and wanting of rewards, as well as a steeper temporal discounting of rewards compared to controls. Moreover, tDCS may be capable to modulate the altered intensity of PD+ICD patients’ liking, but not their altered wanting and temporal discounting of rewards. In Study 3 I investigated whether deficits in reward valuation, commonly reported in schizophrenia, can be observed also in individuals with subclinical psychotic symptoms (PS) to determine if this dysfunction is already present in a potentially pre-psychotic period (Chapter 3). Participants with different levels of subclinical psychotic symptoms (PS) performed effort and temporal discounting tasks. Results showed that aberrant and effort cost computations might be present in individuals with high levels of subclinical PS. In Study 4 I aimed to replicate previous findings of Study 3 and to investigate the neuroimaging correlates, using electroencephalography (EEG), of this abnormal reward valuation in individuals with high levels of PS (Chapter 3). We confirmed that individuals with high PS exhibit altered temporal discounting of rewards relative to individuals with low PS. However, differently from Study 3, high PS participants did not show a greater effort discounting of rewards. Interestingly, even if no differences emerged at a behavioral level, we observed an higher sensitivity to the cost of effort in individuals with high PS (indexed via the LFA, an electrophysiological measure of motivation), but not in those with low PS. In the final chapter I discussed the main findings obtained in my studies in the light of the extant literature (Chapter 4).