Progress in the study of emotion and emotion regulation has increasingly been informed by neuroscientific methods. This article focuses on two components of the event-related potential (ERP)--the P300 and the late positive potential (LPP)--and how they can be used to understand the interaction between the more automatic and controlled processing of emotional stimuli. Research is reviewed exploring: the dynamics of emotional response as indexed at early and late latencies; neurobiological correlates of emotional response; individual and developmental differences; ways in which the LPP can be utilized as a measure of emotion regulation. Future directions for the application of ERP/electroencephalogram (EEG) in achieving a more complete understanding of emotional processing and its regulation are presented.

The ERN is a negative deflection in the event-related potential that peaks approximately 50 ms after the commission of an error. The ERN is thought to reflect early error-processing activity of the anterior cingulate cortex (ACC). First, we review current functional, neurobiological, and developmental data on the ERN. Next, the ERN is discussed in terms of three psychiatric disorders characterized by abnormal response monitoring: anxiety disorders, depression, and substance abuse. These data indicate that increased and decreased error-related brain activity is associated with the internalizing and externalizing dimensions of psychopathology, respectively. Recent data further suggest that abnormal error-processing indexed by the ERN indexes trait- but not state-related symptoms, especially related to anxiety. Overall, these data point to utility of ERN in studying risk for psychiatric disorders, and are discussed in terms of the endophenotype construct.

The error-related negativity (ERN) and error positivity (Pe) are increasingly being examined as neural correlates of response monitoring. The minimum number of error trials included in grand averages varies across studies; indeed, there has not been a systematic investigation on the number of trials required to obtain a stable ERN and Pe. In the current study, the ERN and Pe were quantified as two random trials were added to participants' (N=53) ERP averages. Adding trials increased the correlation with the grand average ERN and Pe; however, high correlations (rs>.80) were obtained with only 6 trials. Internal reliability of the ERN and Pe reached moderate levels after 6 and 2 trials and the signal-to-noise ratio of the ERN and Pe did not change after 8 and 4 trials, respectively. Combined, these data suggest that the ERN and Pe can be quantified using a minimum of between 6 and 8 error trials.

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Emotional stimuli have been shown to elicit increased perceptual processing and attentional allocation. The late positive potential (LPP) is a sustained P300-like component of the event-related potential that is enhanced after the presentation of pleasant and unpleasant pictures as compared with neutral pictures. In this study, the LPP was measured using dense array electroencephalograph both before and after pleasant, neutral, and unpleasant images to examine the time course of attentional allocation toward emotional stimuli. Results from 17 participants confirmed that the LPP was larger after emotional than neutral images and that this effect persisted for 800 ms after pleasant picture offset and at least 1,000 ms after unpleasant picture offset. The persistence of increased attention after unpleasant compared to pleasant stimuli is consistent with the existence of a negativity bias. Overall, these results indicate that attentional capture of emotion continues well beyond picture presentation and that this can be measured with the LPP. Implications and directions for future research are discussed.

IMPORTANCESevere neuropsychiatric conditions, such as schizophrenia, affect distributed neural computations. One candidate system profoundly altered in chronic schizophrenia involves the thalamocortical networks. It is widely acknowledged that schizophrenia is a neurodevelopmental disorder that likely affects the brain before onset of clinical symptoms. However, no investigation has tested whether thalamocortical connectivity is altered in individuals at risk for psychosis or whether this pattern is more severe in individuals who later develop full-blown illness.OBJECTIVES To determine whether baseline thalamocortical connectivity differs between individuals at clinical high risk for psychosis and healthy controls, whether this pattern is more severe in those who later convert to full-blown illness, and whether magnitude of thalamocortical dysconnectivity is associated with baseline prodromal symptom severity. DESIGN, SETTING, AND PARTICIPANTSIn this multicenter, 2-year follow-up, case-control study, we examined 397 participants aged 12-35 years of age (243 individuals at clinical high risk of psychosis, of whom 21 converted to full-blown illness, and 154 healthy controls). The baseline scan dates were January 15, 2010, to April 30, 2012. MAIN OUTCOMES AND MEASURESWhole-brain thalamic functional connectivity maps were generated using individuals' anatomically defined thalamic seeds, measured using resting-state functional connectivity magnetic resonance imaging.RESULTS Using baseline magnetic resonance images, we identified thalamocortical dysconnectivity in the 243 individuals at clinical high risk for psychosis, which was particularly pronounced in the 21 participants who converted to full-blown illness. The pattern involved widespread hypoconnectivity between the thalamus and prefrontal and cerebellar areas, which was more prominent in those who converted to full-blown illness (t 173 = 3.77, P < .001, Hedge g = 0.88). Conversely, there was marked thalamic hyperconnectivity with sensory motor areas, again most pronounced in those who converted to full-blown illness (t 173 = 2.85, P < .001, Hedge g = 0.66). Both patterns were significantly correlated with concurrent prodromal symptom severity (r = 0.27, P < 3.6 × 10 −8 , Spearman ρ = 0.27, P < 4.75 × 10 −5 , 2-tailed).CONCLUSIONS AND RELEVANCE Thalamic dysconnectivity, resembling that seen in schizophrenia, was evident in individuals at clinical high risk for psychosis and more prominently in those who later converted to psychosis. Dysconnectivity correlated with symptom severity, supporting the idea that thalamic connectivity may have prognostic implications for risk of conversion to full-blown illness.

IMPORTANCE A major public health concern associated with schizophrenia and psychotic disorders is the long-term disability that involves impaired cognition, lack of social support, and an inability to function independently in the community. A critical goal of early detection and intervention studies in psychosis is therefore to understand the factors leading to this often profound impairment.OBJECTIVE To develop a predictive model of functional (social and role) outcome in a clinical high-risk sample for psychosis.DESIGN Prospective, naturalistic, longitudinal 3-to 5-year follow-up study.SETTING The Recognition and Prevention Program in New York, a research clinic located in the Zucker Hillside Hospital in New York.PARTICIPANTS One hundred one treatment-seeking patients at clinical high risk for psychosis. Ninety-two (91%) were followed up prospectively for a mean (SD) of 3 (1.6) years. INTERVENTION Neurocognitive and clinical assessment. MAIN OUTCOMES AND MEASURESThe primary outcome variables were social and role functioning at the last follow-up visit. RESULTSPoor social outcome was predicted by reduced processing speed

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