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One of the key features of bipolar disorder (BD) is risky and impulsive decision-making, behaviours theorised to arise from dysregulation in a biobehavioural system governing approach of rewards. However the neural mechanisms of this conceptual model have not been well specified, and there remains a gap between this model and key clinical phenomena such as mixed episodes. This thesis takes a neuroeconomics and reinforcement learning approach to characterise the neural mechanisms of motivational decision-making in BD. A review of the neurobiological evidence for reward dysregulation in BD (Chapter 1) arrives at a model in which striatal hypersensitivity is exacerbated by reduced dorsolateral prefrontal cortical (dlPFC) control. This model is tested by four studies using electrophysiology, source analysis and functional neuroimaging. Chapters 3 and 4 employ EEG to explore how hypomanic traits modulate motivational processing in contexts requiring learning and trade-offs between risk and between immediate and delayed reward. In Chapter 3, high trait hypomania was associated with impaired loss learning and a neural evaluation of rewards and losses more favourably, relative to low hypomania. This “rose-tinted” bias may reinforce risky behaviours that pay off and reduce learning from aversive repercussions. Chapter 4 reports an attentional bias towards immediate reward which may drive a steeper delay discounting trajectory and an inability to delay gratification. In Chapters 5 and 6 simultaneous electrophysiological and functional neuroimaging was utilised to characterise spatial and temporal perturbations to the mesocorticolimbic reward network in a clinical sample of BD. Patients showed a poorer ventromedial prefrontal cortical representation of the objective value of outcomes as well as a heightened striatal reward response. The latter finding was related to decreased dlPFC activation, which also interacted with residual manic symptoms. This is interpreted in terms of reduced top-down executive control that is exacerbated by residual manic symptoms, suggesting a potential mechanism underlying relapse and extremely high levels of reward-seeking seen during mania. EEG source imaging localised differences during reward outcome evaluation to early sensory-attentional (N1), reward evaluation (FRN) and cognitive (P300) stages of processing. For rewards, patients exhibited greater activity in precuneus, frontal eye fields (N1) and ventral anterior cingulate (FRN), consistent with an attentional bias to reward that drives hyperactivity in reward circuitry. Collectively the results provide evidence of reward dysfunction from behavioural measures and two neuroimaging modalities. The results support a model in which a core hypersensitivity to reward and a “rose-tinted” evaluation bias act to 1) potentiate the impact of rewarding outcomes and 2) attenuate aversive ones maintains a distorted representation of objective likelihood and value associated with actions. This is exacerbated by reduced prefrontal control – which may be particularly associated with mania – highlighting a potential target for novel pharmacological and psychological interventions.