Feedback-related brain activity in individual decision: evidence from a gambling EEG study.

In this study, based on scalp electroencephalogram (EEG), we conducted cortical source localization and functional network analyses to investigate the underlying mechanism explaining the decision processes when individuals anticipate maximizing gambling benefits, particularly in situations where the decision outcomes are inconsistent with the profit goals. The findings shed light on the feedback monitoring process, wherein incongruity between outcomes and gambling goals triggers a more pronounced medial frontal negativity and activates the frontal lobe. Moreover, long-range theta connectivity is implicated in processing surprise and uncertainty caused by inconsistent feedback conditions, while middle-range delta coupling reflects a more intricate evaluation of feedback outcomes, which subsequently modifies individual decision-making for optimizing future rewards. Collectively, these findings deepen our comprehension of decision-making under circumstances where the profit goals are compromised by decision outcomes and provide electrophysiological evidence supporting adaptive adjustments in individual decision strategies to achieve maximum benefit.

Edge-centric functional network predicts risk propensity in economic decision-making: evidence from a resting-state fMRI study.

Despite node-centric studies revealing an association between resting-state functional connectivity and individual risk propensity, the prediction of future risk decisions remains undetermined. Herein, we applied a recently emerging edge-centric method, the edge community similarity network (ECSN), to alternatively describe the community structure of resting-state brain activity and to probe its contribution to predicting risk propensity during gambling. Results demonstrated that inter-individual variability of risk decisions correlates with the inter-subnetwork couplings spanning the visual network (VN) and default mode network (DMN), cingulo-opercular task control network, and sensory/somatomotor hand network (SSHN). Particularly, participants who have higher community similarity of these subnetworks during the resting state tend to choose riskier and higher yielding bets. And in contrast to low-risk propensity participants, those who behave high-risky show stronger couplings spanning the VN and SSHN/DMN. Eventually, based on the resting-state ECSN properties, the risk rate during the gambling task is effectively predicted by the multivariable linear regression model at the individual level. These findings provide new insights into the neural substrates of the inter-individual variability in risk propensity and new neuroimaging metrics to predict individual risk decisions in advance.

Multimodal Covariance Network Reflects Individual Cognitive Flexibility.

Cognitive flexibility refers to the capacity to shift between patterns of mental function and relies on functional activity supported by anatomical structures. However, how the brain's structural-functional covarying is preconfigured in the resting state to facilitate cognitive flexibility under tasks remains unrevealed. Herein, we investigated the potential relationship between individual cognitive flexibility performance during the trail-making test (TMT) and structural-functional covariation of the large-scale multimodal covariance network (MCN) using magnetic resonance imaging (MRI) and electroencephalograph (EEG) datasets of 182 healthy participants. Results show that cognitive flexibility correlated significantly with the intra-subnetwork covariation of the visual network (VN) and somatomotor network (SMN) of MCN. Meanwhile, inter-subnetwork interactions across SMN and VN/default mode network/frontoparietal network (FPN), as well as across VN and ventral attention network (VAN)/dorsal attention network (DAN) were also found to be closely related to individual cognitive flexibility. After using resting-state MCN connectivity as representative features to train a multi-layer perceptron prediction model, we achieved a reliable prediction of individual cognitive flexibility performance. Collectively, this work offers new perspectives on the structural-functional coordination of cognitive flexibility and also provides neurobiological markers to predict individual cognitive flexibility.

Brain rhythmic abnormalities in convalescent patients with anti-NMDA receptor encephalitis: a resting-state EEG study.

Objective: Anti-N-methyl-D-aspartate receptor encephalitis (anti-NMDARE) is autoimmune encephalitis with a characteristic neuropsychiatric syndrome and persistent cognition deficits even after clinical remission. The objective of this study was to uncover the potential noninvasive and quantified biomarkers related to residual brain distortions in convalescent anti-NMDARE patients. Methods: Based on resting-state electroencephalograms (EEG), both power spectral density (PSD) and brain network analysis were performed to disclose the persistent distortions of brain rhythms in these patients. Potential biomarkers were then established to distinguish convalescent patients from healthy controls. Results: Oppositely configured spatial patterns in PSD and network architecture within specific rhythms were identified, as the hyperactivated PSD spanning the middle and posterior regions obstructs the inter-regional information interactions in patients and thereby leads to attenuated frontoparietal and frontotemporal connectivity. Additionally, the EEG indexes within delta and theta rhythms were further clarified to be objective biomarkers that facilitated the noninvasive recognition of convalescent anti-NMDARE patients from healthy populations. Conclusion: Current findings contributed to understanding the persistent and residual pathological states in convalescent anti-NMDARE patients, as well as informing clinical decisions of prognosis evaluation.

Repetitive transcranial magnetic stimulation modulates long-range functional connectivity in autism spectrum disorder.

Repetitive transcranial magnetic stimulation (rTMS) is growingly applied in autism spectrum disorder (ASD) due to its potential therapeutic value, however, its effects on functional network configuration and the mechanism underlying clinical improvement are still unclear. In this study, we examined the alternations of functional connectivity induced by rTMS using resting-state electroencephalogram (EEG) in children with ASD. Resting-state EEG was obtained from 24 children with ASD before and after rTMS intervention and from 24 age- and gender-matched typically developing (TD) children. The rTMS intervention course consisted of five 5-s trains at 15 Hz, with 10-min inter-train intervals, on the left parietal lobe each consecutive weekday for 3 weeks (15 sessions in total). Children with ASD showed significantly hypo-connected networks and sub-optimal network properties at both global and local levels, compared with TD peers. After rTMS intervention, long-range intra- and inter-hemispheric connections were significantly promoted, especially those within the alpha band. Meanwhile, network properties at both local and global levels were greatly promoted in the delta, theta, and alpha bands. Consistent with the changes in the network connectivities and properties, the core symptoms in ASD were also relieved measured by clinical scales after treatment. The findings of this study demonstrate that high-frequency rTMS over the parietal lobe is potentially an effective strategy to improve core symptoms by enhancing long-range connectivity reorganization in ASD.

Differentiating Between Alzheimer's Disease and Frontotemporal Dementia Based on the Resting-State Multilayer EEG Network.

Frontotemporal dementia (FTD) is frequently misdiagnosed as Alzheimer's disease (AD) due to similar clinical symptoms. In this study, we constructed frequency-based multilayer resting-state electroencephalogram (EEG) networks and extracted representative network features to improve the differentiation between AD and FTD. When compared with healthy controls (HC), AD showed primarily stronger delta-alpha cross-couplings and weaker theta-sigma cross-couplings. Notably, when comparing the AD and FTD groups, we found that the AD exhibited stronger delta-alpha and delta-beta connectivity than the FTD. Thereafter, by extracting the representative network features and then applying these features in the classification between AD and FTD, an accuracy of 81.1% was achieved. Finally, a multivariable linear regressive model was built, based on the differential topologies, and then adopted to predict the scores of the Mini-Mental State Examination (MMSE) scale. Accordingly, the predicted and actual measured scores were indeed significantly correlated with each other ( r = 0.274, p = 0.036). These findings consistently suggest that frequency-based multilayer resting-state networks can be utilized for classifying AD and FTD and have potential applications for clinical diagnosis.

Transcriptomic and Macroscopic Architectures of Multimodal Covariance Network Reveal Molecular-Structural-Functional Co-alterations.

Human cognition is usually underpinned by intrinsic structure and functional neural co-activation in spatially distributed brain regions. Owing to lacking an effective approach to quantifying the covarying of structure and functional responses, how the structural-functional circuits interact and how genes encode the relationships, to deepen our knowledge of human cognition and disease, are still unclear. Here, we propose a multimodal covariance network (MCN) construction approach to capture interregional covarying of the structural skeleton and transient functional activities for a single individual. We further explored the potential association between brain-wide gene expression patterns and structural-functional covarying in individuals involved in a gambling task and individuals with major depression disorder (MDD), adopting multimodal data from a publicly available human brain transcriptomic atlas and 2 independent cohorts. MCN analysis showed a replicable cortical structural-functional fine map in healthy individuals, and the expression of cognition- and disease phenotype-related genes was found to be spatially correlated with the corresponding MCN differences. Further analysis of cell type-specific signature genes suggests that the excitatory and inhibitory neuron transcriptomic changes could account for most of the observed correlation with task-evoked MCN differences. In contrast, changes in MCN of MDD patients were enriched for biological processes related to synapse function and neuroinflammation in astrocytes, microglia, and neurons, suggesting its promising application in developing targeted therapies for MDD patients. Collectively, these findings confirmed the correlations of MCN-related differences with brain-wide gene expression patterns, which captured genetically validated structural-functional differences at the cellular level in specific cognitive processes and psychiatric patients.

Altered temporal variability in brain functional connectivity identified by fuzzy entropy underlines schizophrenia deficits.

Investigation of the temporal variability of resting-state brain networks informs our understanding of how neural connectivity aggregates and disassociates over time, further shedding light on the aberrant neural interactions that underlie symptomatology and psychosis development. In the current work, an electroencephalogram-based sliding window analysis was utilized for the first time to measure the nonlinear complexity of dynamic resting-state brain networks of schizophrenia (SZ) patients by applying fuzzy entropy. The results of this study demonstrated the attenuated temporal variability among multiple electrodes that were distributed in the frontal and right parietal lobes for SZ patients when compared with healthy controls (HCs). Meanwhile, a concomitant strengthening of the posterior and peripheral flexible connections that may be attributed to the excessive alertness or sensitivity of SZ patients to the external environment was also revealed. These temporal fluctuation distortions combined reflect an abnormality in the coordination of functional network switching in SZ, which is further the source of worse task performance (i.e., P300 amplitude) and the negative relationship between individual complexity metrics and P300 amplitude. Notably, when using the network metrics as features, multiple linear regressions of P300 amplitudes were also exactly achieved for both the SZ and HC groups. These findings shed light on the pathophysiological mechanisms of SZ from a temporal variability perspective and provide potential biomarkers for quantifying SZ's progressive neurophysiological deterioration.

Predicting the long-term after-effects of rTMS in autism spectrum disorder using temporal variability analysis of scalp EEG.

Objective.Repetitive transcranial magnetic stimulation (rTMS) emerges as a useful therapy for autism spectrum disorder (ASD) clinically. Whereas the mechanisms of action of rTMS on ASD are not fully understood, and no biomarkers until now are available to reliably predict the follow-up rTMS efficacy in clinical practice.Approach.In the current work, the temporal variability was investigated in resting-state electroencephalogram of ASD patients, and the nonlinear complexity of related time-varying networks was accordingly evaluated by fuzzy entropy.Main results.The results showed the hyper-variability in the resting-state networks of ASD patients, while three week rTMS treatment alleviates the hyper fluctuations occurring in the frontal-parietal and frontal-occipital connectivity and further contributes to the ameliorative ASD symptoms. In addition, the changes in variability network properties are closely correlated with clinical scores, which further serve as potential predictors to reliably track the long-term rTMS efficacy for ASD.Significance.The findings consistently demonstrated that the temporal variability of time-varying networks of ASD patients could be modulated by rTMS, and related variability properties also help predict follow-up rTMS efficacy, which provides the potential for formulating individualized treatment strategies for ASD (ChiCTR2000033586).