The monetary incentive delay (MID) task has been widely used in fMRI studies to investigate the neural networks involved in anticipatory and consummatory reward processing. Previous efforts to adapt the MID task for use with ERPs, however, have had limited success. Here, we sought to further decompose reward dynamics using a comprehensive set of anticipatory (cue-N2, cue-P3, contingent negative variation [CNV]) and consummatory ERPs (feedback negativity [FN], feedback P3 [fb-P3]). ERP data was recorded during adapted versions of the MID task across two experiments. Unlike previous studies, monetary incentive cues modulated the cue-N2, cue-P3, and CNV; however, cue-related ERPs and the CNV were uncorrelated with one another, indicating distinct anticipatory subprocesses. With regard to consummatory processing, FN amplitude primarily tracked outcome valence (reward vs. nonreward), whereas fb-P3 amplitude primarily tracked outcome salience (uncertain vs. certain). Independent modulation of the cue-P3 and fb-P3 was observed, indicating that these two P3 responses may uniquely capture the allocation of attention during anticipatory and consummatory reward processing, respectively. Overall, across two samples, consistent evidence of both anticipatory and consummatory ERP activity was observed on an adapted version of the MID paradigm, demonstrating for the first time how these ERP components may be integrated with one another to more fully characterize the time course of reward processing. This ERP-MID paradigm is well suited to parsing reward dynamics, and can be applied to both healthy and clinical populations.

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In neuroeconomics, valuation refers to the process of assigning values to states and actions based on the animal’s current representation of the environment while reward processing corresponds to processing the feedback received from the environment to update the values of states and actions. In this article, we review the brain circuits associated with valuation and reward processing and argue that these are fundamental processes critical in many cognitive functions. Specifically, we focus on the role of valuation and reward processing in attention, memory, decision–making, and learning. Next, the extant neuroimaging literature on a number of psychiatric disorders is reviewed (i.e., addiction, pathological gambling, schizophrenia, and mood disorders), and an argument is made that associated deficits in cognitive functions can be explained in terms of abnormal valuation and reward processing. The review concludes with the impact of this framework in clinical settings and prescriptions for future research, in particular with regards to the conversions of qualitatively different valuation systems into a system of common currency.

Mismatch negativity (MMN) amplitude has been widely shown to be diminished in schizophrenia and, more recently, in other psychotic disorders. Although there is considerable evidence linking MMN reduction to cognitive and functional deficits in schizophrenia, there is little evidence of associations with specific psychotic symptoms. Further, it is unclear if MMN reductions relate to specific symptoms, cognitive, and functional deficits transdiagnostically across different psychotic disorders. The present study examines MMN amplitude in a large cohort of cases diagnosed with psychotic disorders including schizophrenia and schizoaffective disorder (N = 116); bipolar disorder and major depressive disorder (N = 75); and other psychotic disorders (N = 25), as well as individuals with no psychotic disorder diagnoses (N = 248). Furthermore, we examined the association of MMN with symptoms, cognitive functioning, and real-world functioning to determine whether these relationships differ by diagnosis. Results showed that MMN amplitude was reduced in cases overall compared to never-psychotic individuals, with no differences between psychotic disorders. Furthermore, there were transdiagnostic associations of reduced duration MMN (MMN-D) with worse auditory hallucinations (r = .14) and disorganization (r = .14), frequency MMN (MMN-F) with real-word functioning (r = .20) and episodic memory (r = −.22), and both components with executive functioning (MMN-D: r = −.17; MMN-F: r = −.15). Our findings relating MMN reductions with cognitive and real-world functioning replicate earlier research in schizophrenia and extend these relationships to other psychotic disorders. Furthermore, our correlations with MMN-D are consistent with computational modeling research and theoretical proposals that view MMN reduction, cognitive dysfunction, and psychotic symptoms as reflecting underlying predictive coding deficits. However, differences in relationships with MMN-F suggest that additional work is warranted on this topic.