Event-related potentials of social comparisons in depression and social anxiety.

Social comparison is central in human life and can be especially challenging in depression and social anxiety. We assessed event-related potentials and emotions using a social comparison task in which participants received feedback on both their own and a co-player's performance, in participants with depression and/or social anxiety (n = 63) and healthy controls (n = 72). Participants reported more negative emotions for downward (being better than the co-player [participant correct, co-player wrong]) and upward (being worse than the co-player [participant wrong, co-player correct]) comparisons versus even outcomes, with these effects being stronger in depression and social anxiety. At the Medial Frontal Negativity, both controls and depressed participants showed a more negative amplitude for upward comparison versus both the participant and co-player performing wrong. Socially anxious subjects showed the opposite effect, possibly due to greater expectations about being worse than others. The P300 decreased for downward and upward comparisons compared to even outcomes, which may relate to the higher levels of conflict of social inequality. Depressed and socially anxious subjects showed a blunted P300 increase over time in response to the task outcomes, suggesting deficits in allocating resources for the attention of incoming social information. The LPP showed increased amplitude for downward and upward comparison versus the even outcomes and no group effect. Emotional findings suggest that social comparisons are more difficult for depressed and socially anxious individuals. Event-related potentials findings may shed light on the neural substrates of these difficulties.

Event-related potentials during the ultimatum game in people with symptoms of depression and/or social anxiety.

Depression and social anxiety are common disorders that have a profound impact on social functioning. The need for studying the neural substrates of social interactions in mental disorders using interactive tasks has been emphasized. The field of neuroeconomics, which combines neuroscience techniques and behavioral economics multiplayer tasks such as the Ultimatum Game (UG), can contribute in this direction. We assessed emotions, behavior, and Event-Related Potentials in participants with depression and/or social anxiety symptoms (MD/SA, n = 63, 57 females) and healthy controls (n = 72, 67 females), while they played the UG. In this task, participants received fair, mid-value, and unfair offers from other players. Mixed linear models were implemented to assess trial level changes in neural activity. The MD/SA group reported higher levels of sadness in response to mid-value and unfair offers compared to controls. In controls, the Medial Frontal Negativity associated with fair offers increased over time, while this dynamic was not observed in the MD/SA group. The MD/SA group showed a decreased P3/LPP in all offers, compared to controls. These results indicate an enhanced negative emotional response to unfairness in the MD/SA group. Neural results reveal a blunted response over time to positive social stimuli in the MD/SA group. Moreover, between-group differences in P3/LPP may relate to a reduced saliency of offers and/or to a reduced availability of resources for processing incoming stimuli in the MD/SA group. Findings may shed light into the neural substrates of social difficulties in these disorders.

Neural processing of iterated prisoner's dilemma outcomes indicates next-round choice and speed to reciprocate cooperation.

The iterated prisoner's dilemma (iPD) game is a well-established model for testing how people cooperate, and the neural processes that unfold after its distinct outcomes have been partly described. Recent theoretical models suggest evolution favors intuitive cooperation, which raises questions on the behavioral but also neural timelines involved. We studied the outcome/feedback stage of iPD rounds with electroencephalography (EEG) methods. Results showed that neural signals associated with this stage also relate to future choice, in an outcome-dependent manner: (i) after zero-gain "sucker's payoffs" (unreciprocated cooperation), a participant's decision thereafter relates to changes to the feedback-related negativity (FRN); (ii) after one-sided non-cooperation (participant wins at co-player's expense), by the P3; (iii) after mutual cooperation, by late frontal delta-band modulations. Critically, faster reciprocation behavior towards a co-player's choice to cooperate was predicted, on a single-trial basis, by players' P3 and frontal delta modulations at the immediately preceding trial. Delta-band signaling is discussed in relation to homeostatic regulation processing in the literature. The findings relate the early outcome/feedback stage to subsequent decisional processes in the iPD, providing a first neural account of the brief timelines implied in heuristic modes of cooperation.

Social avoidance in depression: A study using a social decision-making task.

Depression significantly affects interpersonal functioning. Social avoidance may play an important role in depression, limiting opportunities and social skills acquisition, contributing to the maintenance of social difficulties. In the last few years, the need for studying social interactions using interactive tasks has been highlighted. This study investigated social avoidance in unmedicated depressed (n = 26) and matched healthy control (n = 26) participants, using a novel computerized social decision-making task (the TEAM task). In this task, participants choose between a social option (playing in a team with a coplayer) and an individual option (playing alone). Although the social option is more profitable from a material point of view, it can also be challenging because of social comparison and guilt feelings for failing the team. It was found that the higher the rank of the coplayer, the stronger the negative emotions (shame, guilt) reported by participants and the more they opted for the individual option. Depressed participants reported significantly less positive (happiness) and more negative (shame, guilt, disappointment) feelings regarding the task. Importantly, depressed participants chose the individual option significantly more often than controls, which led to lower gains in this group. Furthermore, as the task progressed, controls selected the individual option less often, whereas depressed participants selected the individual option more often. Our findings illustrate the importance of social avoidance in depression and how this behavior can lead to negative consequences. They also highlight the role of social comparison and guilt-related processes in underlying social avoidance in depression. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Nonlinear complexity analysis of brain FMRI signals in schizophrenia.

We investigated the differences in brain fMRI signal complexity in patients with schizophrenia while performing the Cyberball social exclusion task, using measures of Sample entropy and Hurst exponent (H). 13 patients meeting diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM IV) criteria for schizophrenia and 16 healthy controls underwent fMRI scanning at 1.5 T. The fMRI data of both groups of participants were pre-processed, the entropy characterized and the Hurst exponent extracted. Whole brain entropy and H maps of the groups were generated and analysed. The results after adjusting for age and sex differences together show that patients with schizophrenia exhibited higher complexity than healthy controls, at mean whole brain and regional levels. Also, both Sample entropy and Hurst exponent agree that patients with schizophrenia have more complex fMRI signals than healthy controls. These results suggest that schizophrenia is associated with more complex signal patterns when compared to healthy controls, supporting the increase in complexity hypothesis, where system complexity increases with age or disease, and also consistent with the notion that schizophrenia is characterised by a dysregulation of the nonlinear dynamics of underlying neuronal systems.

Abnormal brain activity during a reward and loss task in opiate-dependent patients receiving methadone maintenance therapy.

A core feature of human drug dependency is persistence in seeking and using drugs at the expense of other life goals. It has been hypothesized that addiction is associated with overvaluation of drug-related rewards and undervaluation of natural, nondrug-related rewards. Humans additionally tend to persist in using drugs despite adverse consequences. This suggests that the processing of both rewarding and aversive information may be abnormal in addictions. We used fMRI to examine neural responses to reward and loss events in opiate-dependent patients receiving methadone maintenance treatment (MMT, n=30) and healthy controls (n=23) using nondrug-related stimuli. Half of the patients were scanned after/before daily methadone intake (ADM/BDM patient groups). During reward trials, patients as a whole exhibited decreased neural discrimination between rewarding and nonrewarding outcomes in the dorsal caudate. Patients also showed reduced neural discrimination in the ventral striatum with regard to aversive and nonaversive outcomes and failed to encode successful loss avoidance as a reward signal in the ventral striatum. Patients also showed decreased insula activation during the anticipation/decision phase of loss events. ADM patients exhibited increased loss signals in the midbrain/parahippocampal gyrus, possibly related to a disinhibition of dopamine neurons. This study suggests that patients with opiate dependency on MMT exhibit abnormal brain activations to nondrug-related rewarding and loss events. Our findings add support to proposals that treatments for opiate addiction should aim to increase the reward value of nondrug-related rewarding events and highlight the importance of potential abnormalities in aversive information processing.

Salience network-midbrain dysconnectivity and blunted reward signals in schizophrenia.

Theories of schizophrenia propose that abnormal functioning of the neural reward system is linked to negative and psychotic symptoms, by disruption of reward processing and promotion of context-independent false associations. Recently, it has been argued that an insula-anterior cingulate cortex (ACC) salience network system enables switching of brain states from the default mode to a task-related activity mode. Abnormal interaction between the insula-ACC system and reward processing regions may help explain abnormal reinforcer processing and symptoms. Here we use functional magnetic resonance imaging to assess the neural correlates of reward processing in schizophrenia. Furthermore, we investigated functional connectivity between the dopaminergic midbrain, a key region for the processing of reinforcers, and other brain regions. In response to rewards, controls activated task related regions (striatum, amygdala/hippocampus and midbrain) and the insula-ACC salience network. Patients similarly activated the insula-ACC salience network system but failed to activate task related regions. Reduced functional connectivity between the midbrain and the insula was found in schizophrenia, with the extent of this abnormality correlating with increased psychotic symptoms. The findings support the notion that reward processing is abnormal in schizophrenia and highlight the potential role of abnormal interactions between the insula-ACC salience network and reward regions.

Abnormal neural responses to social exclusion in schizophrenia.

Social exclusion is an influential concept in politics, mental health and social psychology. Studies on healthy subjects have implicated the medial prefrontal cortex (mPFC), a region involved in emotional and social information processing, in neural responses to social exclusion. Impairments in social interactions are common in schizophrenia and are associated with reduced quality of life. Core symptoms such as delusions usually have a social content. However little is known about the neural underpinnings of social abnormalities. The aim of this study was to investigate the neural substrates of social exclusion in schizophrenia. Patients with schizophrenia and healthy controls underwent fMRI while participating in a popular social exclusion paradigm. This task involves passing a 'ball' between the participant and two cartoon representations of other subjects. The extent of social exclusion (ball not being passed to the participant) was parametrically varied throughout the task. Replicating previous findings, increasing social exclusion activated the mPFC in controls. In contrast, patients with schizophrenia failed to modulate mPFC responses with increasing exclusion. Furthermore, the blunted response to exclusion correlated with increased severity of positive symptoms. These data support the hypothesis that the neural response to social exclusion differs in schizophrenia, highlighting the mPFC as a potential substrate of impaired social interactions.

Expected value and prediction error abnormalities in depression and schizophrenia.

The dopamine system has been linked to anhedonia in depression and both the positive and negative symptoms of schizophrenia, but it remains unclear how dopamine dysfunction could mechanistically relate to observed symptoms. There is considerable evidence that phasic dopamine signals encode prediction error (differences between expected and actual outcomes), with reinforcement learning theories being based on prediction error-mediated learning of associations. It has been hypothesized that abnormal encoding of neural prediction error signals could underlie anhedonia in depression and negative symptoms in schizophrenia by disrupting learning and blunting the salience of rewarding events, and contribute to psychotic symptoms by promoting aberrant perceptions and the formation of delusions. To test this, we used model based functional magnetic resonance imaging and an instrumental reward-learning task to investigate the neural correlates of prediction errors and expected-reward values in patients with depression (n=15), patients with schizophrenia (n=14) and healthy controls (n=17). Both patient groups exhibited abnormalities in neural prediction errors, but the spatial pattern of abnormality differed, with the degree of abnormality correlating with syndrome severity. Specifically, reduced prediction errors in the striatum and midbrain were found in depression, with the extent of signal reduction in the bilateral caudate, nucleus accumbens and midbrain correlating with increased anhedonia severity. In schizophrenia, reduced prediction error signals were observed in the caudate, thalamus, insula and amygdala-hippocampal complex, with a trend for reduced prediction errors in the midbrain, and the degree of blunting in the encoding of prediction errors in the insula, amygdala-hippocampal complex and midbrain correlating with increased severity of psychotic symptoms. Schizophrenia was also associated with disruption in the encoding of expected-reward values in the bilateral amygdala-hippocampal complex and parahippocampal gyrus, with the degree of disruption correlating with psychotic symptom severity. Neural signal abnormalities did not correlate with negative symptom severity in schizophrenia. These findings support the suggestion that a disruption in the encoding of prediction error signals contributes to anhedonia symptoms in depression. In schizophrenia, the findings support the postulate of an abnormality in error-dependent updating of inferences and beliefs driving psychotic symptoms. Phasic dopamine abnormalities in depression and schizophrenia are suggested by our observation of prediction error abnormalities in dopamine-rich brain areas, given the evidence for dopamine encoding prediction errors. The findings are consistent with proposals that psychiatric syndromes reflect different disorders of neural valuation and incentive salience formation, which helps bridge the gap between biological and phenomenological levels of understanding.

The role of hippocampal atrophy in depression: a neurocomputational approach.

The role of hippocampal atrophy in the pathogenesis of major depression remains under investigation. Here, we show, within a neural network model, that the incorporation of atrophy reproduces the changes observed in cognitive impairment in depression and could also contribute to the maintenance of the depressed mood. Some other clinical observations, such as treatment resistance and frequent relapses of illness, could also be explained within the framework of the model. We also simulate the action of cognitive therapy and a combined treatment of cognitive therapy and antidepressant drugs. Our findings suggest that, in the presence of hippocampal atrophy, the incorporation of antidepressant drugs would be necessary for the reversal of symptomatology.