Cannabis use is rising in the United States. Up to 30 % of individuals who use cannabis develop cannabis use disorder (CUD), for which there are no FDA-approved treatments. This randomized controlled trial (RCT) evaluated the feasibility and efficacy of a novel, one-month telehealth intervention of remotely supervised tDCS (RS-tDCS) paired with mindfulness meditation. This home-based telehealth intervention was evaluated in a cohort of women with multiple sclerosis (MS), a vulnerable subpopulation of adults with high rates of CUD.

The intervention included 20 home-based RS-tDCS sessions targeting the left DLPFC, delivering 2.0mA for 20minutes, paired with guided mindfulness meditation. Sessions were conducted 5 days per week for four weeks. Fifty-two women with MS and CUD (age: 44 ± 10 years) consented to participate; 47 were randomized 2:1 to active or sham tDCS. Feasibility was assessed via retention and adherence, while preliminary efficacy was measured by cannabis use, withdrawal symptoms, and MS-related symptom scales.

Of 47 randomized participants (31 active, 16 sham), 39 (83 %) completed the intervention. The active tDCS group showed significant reductions in weekly cannabis use (Daily Sessions, Frequency, Age of Onset, and Quantity of Cannabis Use Inventory, DFAQ-CU: 5.3 ± 2.4 vs. 3.9 ± 2.7 days, p = 0.014) and withdrawal symptoms (CWS: p < 0.001). A trend toward reduced MS-related symptoms was observed (SymptoMScreen: p = 0.031). Cognitive performance improvement at the end of the intervention was significant in the active group (p = 0.011 vs. p = 0.172), supporting functional benefits of reduced cannabis use.

This pilot RCT supports the feasibility and preliminary efficacy of telehealth tDCS in a medical subpopulation. Studying women with MS highlights its potential for large-scale RCTs and clinical use.

Currently, the neural mechanisms underlying the topological changes in the brains of individuals with depressive tendencies and the decline in their emotion regulation abilities remain largely unknown. Therefore, this study investigates resting-state brain network characteristics in college students with depressive tendencies (DT) and their preference to cognitive reappraisal strategies.

A group of 38 DT students and 41 healthy controls (HCs) were assessed using questionnaires on cognitive reappraisal sub-strategies, followed by alpha and beta frequency band EEG feature extraction.

Through complex network analysis, DT participants showed significantly reduced preferences for positive reappraisal and detached reappraisal compared to HCs, while exhibiting higher preferences for involved reappraisal and negative reappraisal. Additionally, abnormalities in brain network centrality were observed, particularly in the frontal and limbic lobes across various frequency bands. A significant correlation was found between the preference for cognitive reappraisal sub-strategies in DT participants and significant changes in graph indices.

The findings highlight substantial alterations in the resting-state brain networks of DT individuals, closely associated with cognitive reappraisal strategy preferences. These alterations may affect emotion regulation strategy choices, offering insights into the neural mechanisms of emotional regulation difficulties in DT.

Background: Post-traumatic stress disorder (PTSD) manifests through distinct symptom clusters that can respond differently to treatments. Neurofeedback guided by the Amygdala-derived-EEG-fMRI-Pattern (Amyg-EFP-NF) has been utilized to train PTSD patients to regulate amygdala-related activity and decrease symptoms. Methods: We conducted a combined analysis of 128 PTSD patients from three clinical trials of Amyg-EFP-NF to evaluate effects across symptom clusters (as assessed by CAPS-5 subscales) and on emotion regulation processing (evaluated by the ERQ). Results: Amyg-EFP-NF significantly reduced severity across all PTSD symptom clusters immediately post-treatment, with improvements maintained at three-month follow-up. The arousal and reactivity cluster showed continued significant improvement during follow-up. Combined effect sizes were large (η2p = 0.23-0.35) across all symptom clusters. Regression analysis revealed that emotion regulation processes significantly explained 17% of the variance in symptom improvement during the follow-up period. Conclusions: Reduction of PTSD symptoms following Amyg-EFP-NF occurs across all symptom clusters, with emotional regulation processes potentially serving as an underlying mechanism of action. These results support Amyg-EFP-NF as a comprehensive treatment approach for PTSD that continues to show benefits after treatment completion.

Psychological pain is the most important factor affecting suicide rates. However, the factors contributing to psychological pain in medical students remain poorly understood.

This study aimed to investigate the effects of a stress mindset on psychological pain and the mediating roles of cognitive reappraisal and self-identity among Chinese medical students.

Medical students (N = 2056; 1,369, 66.60% female; 683, 33.40% male) from China completed multiple measures of stress mindset, self-identity, cognitive reappraisal, and psychological pain. Correlation and mediation analyses were conducted using SPSS 29.0 and Mplus 8.3.

(1) The stress mindset was significantly negatively correlated with psychological pain among medical students. (2) Cognitive reappraisal mediated the relationship between the stress mindset and psychological pain. (3) Self-identity mediated the relationship between the stress mindset and psychological pain. (4) Cognitive reappraisal and self-identity jointly mediated the relationship between the stress mindset and psychological pain.

The results of this study deepen the understanding of the psychological processes linking stress mindset and psychological pain and provide a valuable reference for reducing psychological pain and improving the well-being of medical students.

People with bipolar disorder (BD) present with mood instability resulting from more frequent and intense emotions in response to environmental conditions relative to healthy subjects. The aim of this study was to investigate the time course of emotion regulation strategies, distraction, and reappraisal in euthymic BD patients (i.e., normal mood range) using electroencephalography (EEG). Fourteen BD patients and 13 matched healthy controls took part in an experiment constituting three conditions, i.e., a passive viewing of positive, negative, and neutral pictures, and two regulation conditions, one with a reappraisal strategy and the other with a distraction strategy. Critically, the ERP results indicated that during passive viewing, the Late Positive Potential (LPP) was larger in BD patients compared with healthy controls, but only for neutral pictures. During emotion regulation, LPP amplitude was reduced in distraction conditions compared with viewing ones, especially for negative emotions in both patients and controls. Importantly, LPP was reduced in reappraisal conditions compared with passive viewing in an early time window for negative emotions and in a later time window for positive emotions in controls but not in patients. Our findings showed that the temporal dynamics of emotion regulation by reappraisal are faster for negative than for positive emotions in controls but not in BD patients.

The ventrolateral prefrontal cortex (VLPFC) plays a pivotal role in emotion regulation, yet the effectiveness of neurofeedback (NF) training targeting the VLPFC remains uncertain, suggesting significant individual differences in outcomes. In this study, we aimed to clarify these differences by enrolling 90 participants, randomly assigned to either an experimental group or a sham group (n = 48/42). Participants in the experimental group underwent VLPFCNF training over eight sessions across two consecutive days, while those in the sham group received random signals from functional near-infrared spectroscopy (fNIRS). To investigate individual variability, participants in the experimental group were further categorized as high or low-efficacy groups based on their training efficiency, determined by the regression slope of VLPFC activity over the sessions. Our results revealed a significant reduction in negative emotions and increased VLPFC activity during emotion regulation in the high-efficacy group, compared to both the low-efficacy group and sham group. Importantly, the benefit in emotion regulation, as reflected by decreased negativity ratings, was predicted by NF training efficiency. Furthermore, the enhancement of VLPFC activity during emotion regulation fully mediated the relationship between NF training efficiency and emotion regulation benefits. Participants with higher VLPFCNF training efficiency exhibited greater engagement of the VLPFC during emotion regulation, leading to superior emotional outcomes. Additionally, VLPFCNF training efficiency was linked to the habitual use of reappraisal strategies in daily life. This study provides novel causal evidence that VLPFCNF training can effectively enhance emotion regulation, highlighting the importance of individual differences in training outcomes. Our findings suggest that NF training targeting the VLPFC offers a promising and personalized intervention strategy for improving emotion regulation, with potential applications for treating emotional disorders. This research underscores the potential of personalized NF approaches, offering new avenues for tailored therapeutic interventions in the future.

Repetitive drug use results in enduring structural and functional changes in the brain. Addiction research has consistently revealed significant modifications in key brain networks related to reward, habit, salience, executive function, memory and self-regulation. Techniques like Voxel-based Morphometry have highlighted large-scale structural differences in grey matter across distinct groups. Source-based Morphometry (SBM) takes this a step further by incorporating the Independent Component Analysis to detect shared patterns of grey matter variation, all without requiring prior selection of regions of interest. However, SBM has yet to be employed in the study of structural alteration patterns related to cocaine addiction. Therefore, we performed this analysis to explore alterations in structural covariance specific to cocaine addiction. Our study involved 40 individuals diagnosed with Cocaine Use Disorder (CUD) and 40 matched healthy controls. Participants with CUD completed clinical questionnaires assessing the severity of their dependence and other relevant clinical variables. Following the adjustment for age-related effects, we observed notable disparities between groups in two structural independent components, which we identified as the structural cerebellar network and the structural lateral frontoparietal network, which display opposing trends. Specifically, the individuals with CUD exhibited a heightened contribution to the cerebellar network but simultaneously demonstrated a reduced contribution to the lateral frontoparietal network compared to the healthy controls. These findings unveil distinctive covariance patterns of neuroregulation linked with cocaine addiction, which indicates an interruption in the typical structural development in an affected lateral frontoparietal network, while suggesting an extended pattern of neuroregulation within the cerebellar network in individuals with CUD.

Experiencing trauma or other adverse life events is highly prevalent and poses a significant risk for the development of mental disorders. Understanding the underlying mechanisms and neural processes involved in trauma processing is crucial for both prevention and targeting symptoms. Especially, difficulties in emotion regulation emerge as one key mechanism implicated in the development of conditions such as post-traumatic stress disorder (PTSD) following traumatic experiences. However, neural correlates of explicit emotion regulation among individuals who have undergone trauma have not received much attention. Understanding the neural basis of dysregulated emotion following trauma could reveal important details about how trauma interferes with emotional regulation systems, informing the development of more specific intervention approaches. Therefore, this mini review summarizes current research, and identifies relevant gaps in the literature and challenges for future studies. Specifically, it provides an overview of the neural dysregulation associated with explicit emotion regulation strategies such as reappraisal or suppression. Finally, it highlights promising findings from intervention studies targeting emotion regulation, such as trauma-focused exposure therapy and neurofeedback, indicating neural plasticity in individuals with traumatic experiences. Hereby, this review aims to bridge the gap between fundamental and intervention research and highlights future directions for translational research.

Impaired emotion regulation has been proposed as a putative endophenotype in bipolar disorder (BD). Functional magnetic resonance imaging (fMRI) studies investigating this in unaffected first-degree relatives (UR) have thus far yielded incongruent findings. Hence, the current paper examines neural subgroups among UR during emotion regulation.

71 UR of patients with BD and 66 healthy controls (HC) underwent fMRI scanning while performing an emotion regulation task. Hierarchical cluster analysis was performed on extracted signal change during emotion down-regulation in pre-defined regions of interest (ROIs). Identified subgroups were compared on neural activation, demographic, clinical, and cognitive variables.

Two subgroups of UR were identified: subgroup 1 (39 UR; 55%) was characterized by hypo-activity in the dorsolateral, dorsomedial, and ventrolateral prefrontal cortex and the bilateral amygdalae, but comparable activation to HC in the other ROIs; subgroup 2 (32 UR; 45%) was characterized by hyperactivity in all ROIs. Subgroup 1 had lower success in emotion regulation compared to HC and reported more childhood trauma compared to subgroup 2 and HC. Subgroup 2 reported more anxiety, lower functioning, and greater attentional vigilance toward fearful faces compared to HC. Relatives from both subgroups were poorer in recognizing positive faces compared to HC.

These findings may explain the discrepancy in earlier fMRI studies on emotion regulation in UR, showing two different subgroups of UR that both exhibited aberrant neural activity during emotion regulation, but in opposite directions. Furthermore, the results suggest that impaired recognition of positive facial expressions is a broad endophenotype of BD.

Childhood maltreatment is an established risk factor for psychopathology. However, it remains unclear how childhood traumatic events relate to mental health problems and how the brain is involved. This study examined the serial mediation effect of brain morphological alterations and emotion-/reward-related functions on linking the relationship from maltreatment to depression. We recruited 156 healthy adolescents and young adults and an additional sample of 31 adolescents with major depressive disorder for assessment of childhood maltreatment, depressive symptoms, cognitive reappraisal and anticipatory/consummatory pleasure. Structural MRI data were acquired to identify maltreatment-related cortical and subcortical morphological differences. The mediation models suggested that emotional maltreatment of abuse and neglect, was respectively associated with increased gray matter volume in the ventral striatum and greater thickness in the middle cingulate cortex. These structural alterations were further related to reduced anticipatory pleasure and disrupted cognitive reappraisal, which contributed to more severe depressive symptoms among healthy individuals. The above mediating effects were not replicated in our clinical group partly due to the small sample size. Preventative interventions can target emotional and reward systems to foster resilience and reduce the likelihood of future psychiatric disorders among individuals with a history of maltreatment.

Loneliness, distress from having fewer social contacts than desired, has been recognized as a significant public health crisis. Although a substantial body of research has established connections between loneliness and various forms of psychopathology, our understanding of the neural underpinnings of loneliness in schizophrenia spectrum disorders (SSD) and major depressive disorder (MDD) remains limited.

In this study, structural magnetic resonance imaging (sMRI) data were collected from 57 SSD and 45 MDD patients as well as 41 healthy controls (HC). Loneliness was measured with the German version of the University of California, Los Angeles Loneliness Scale (UCLA-LS). We used FreeSurfer v7.2 for automated parcellation of cortical regions.

SSD patients showed reduced cortical volume and thickness in fronto-parietal and temporal regions when compared to HC (p < 0.05, Benjamini-Hochberg (BH) corr.). In SSD, volume of the right superior temporal gyrus was associated with UCLA-LS total score (p = 0.030; BH corr.). MDD patients showed reduced cortical volume and thickness in fronto-parietal regions (p < 0.05, BH corr.). In MDD, cortical thickness of the right superior parietal cortex was associated with UCLA-LS total score (p = 0.038; BH corr.).

Our study suggests a different neural signature of loneliness in patients with SSD and MDD, comprising temporal and parietal regions responsible for social and attentive processing. Identifying neurobiological mechanisms underlying loneliness is critical for understanding its role in severe mental illnesses and identifying potential therapeutic targets.

Emotional dysregulation is a serious and impairing mental health problem. We examined functional activity and connectivity of neural networks involved in emotional dysregulation at baseline and following a pilot neurostimulation-enhanced cognitive restructuring intervention in a transdiagnostic clinical adult sample.

Neuroimaging data were analyzed from adults who scored 89 or higher on the Difficulties with Emotion Regulation (DERS) scale and had at least one DSM-5 diagnosis. These participants were part of a pilot randomized, double-blind, placebo-controlled trial combining a single therapeutic session of cognitive restructuring with active or sham transcranial magnetic stimulation over the dorsolateral prefrontal cortex. During the study, participants engaged in an emotional regulation task using personalized autobiographical stressors while undergoing functional magnetic resonance imaging (fMRI) before and after the pilot intervention. The fMRI task required participants to either experience the emotions associated with the memories or apply cognitive restructuring strategies to reduce their distress.

Whole-brain fMRI results during regulation at baseline revealed increased activation in the dorsal frontoparietal network but decreased activation in the supplementary motor area, cingulate cortex, insula, and ventrolateral prefrontal cortex (vlPFC). Emotion dysregulation was associated with greater vmPFC and amygdala activation and functional connectivity between these regions. The strength of functional connectivity between the dlPFC and other frontal regions was also a marker of emotional dysregulation. Preliminary findings from a subset of participants who completed the follow-up fMRI scan showed that active neurostimulation improved behavioral indices of emotion regulation more than sham stimulation. A whole-brain generalized psychophysiological interaction analysis indicated that active neurostimulation selectively increased occipital cortex connectivity with both the insula and the dlPFC. Region-of-interest functional connectivity analyses showed that active neurostimulation selectively increased dlPFC connectivity with the insula and orbitofrontal cortex (OFC).

Insufficient neural specificity during the emotion regulation process and over-involvement of frontal regions may be a marker of emotional dysregulation across disorders. OFC, vlPFC, insula activity, and connectivity are associated with improved emotion regulation in transdiagnostic adults. In this pilot study, active neurostimulation led to neural changes in the emotion regulation network after a single session; however, the intervention findings are preliminary, given the small sample size. These functional network properties can inform future neuroscience-driven interventions and larger-scale studies.

Emotional dysregulation, particularly unconscious catastrophic cognitions, plays a pivotal role in the genesis of panic disorder (PD). However, no studies have yet applied the percentage of amplitude fluctuation (PerAF) metric in resting-state functional magnetic resonance imaging to examine spontaneous neural functioning and its relation to catastrophic cognitions in PD.

To explore the interplay between resting-state neural activity, functional connectivity (FC), and unconscious emotion regulation in individuals with PD.

Cross-sectional study.

The study encompassed 51 participants, including 26 PD patients and 25 healthy individuals. The PerAF algorithm was employed to explore the local spontaneous neural activity in PD. Regions exhibiting aberrant spontaneous neural activity were used as seed points for whole-brain FC analysis. Correlations were utilized to examine associations between local neural activity patterns and neurocognitive assessments in PD.

The study revealed that compared to healthy individuals, PD patients exhibited elevated PerAF values in key emotion-regulation-related brain regions, including the ventromedial prefrontal cortex (vmPFC), striatum, amygdala, dorsomedial prefrontal cortex (dmPFC), and cerebellum. In addition, the resting-state FC between vmPFC and precuneus, as well as between the cerebellum and precuneus, was weakened in PD patients. Furthermore, positive associations were noted between PerAF measurements of vmPFC and amygdala and catastrophizing scores.

PD involves regional and network-level alterations in resting-state brain activity. The fronto-striatal-limbic circuits play a critical role in catastrophic-style emotion regulation in PD patients. Reduced FC within the default mode network and cerebellum-default mode network may signify a coordination anomaly in introspection and cognitive activities in PD. These findings complement the model of implicit emotion regulation in PD and suggest potential intervention targets.

We examine the association between stress exposure during early development (i.e., the prenatal period through the first two postnatal years) and variation in brain structure and function relevant to anxiety. Evidence of stress-related effects occurring in regions essential for emotional processing and regulation may increase susceptibility to anxiety.

Cognitive theories emphasize the central role of anger and anger suppression in obsessive-compulsive disorder (OCD). According to these theories, anger suppression is seen as a consequence of OCD, whereas cognitive beliefs, such as an inflated sense of responsibility, are seen as antecedent factors. To extend the findings from cross-sectional studies, the current study investigated the temporal associations between OCD symptoms, an inflated sense of responsibility, and anger suppression. Consistent with cognitive considerations, we hypothesized that OCD symptoms mediate the association between feelings of responsibility and anger suppression. These associations were also explored in patients presenting particularly high checking-related symptoms. Further, the stability of effects beyond controlling for depressive symptoms and medication intake was explored.

A total of N = 48 patients with OCD (50% female, M = 32.46 [SD = 10.63] years of age) completed measures on obsessive beliefs, OCD symptoms, and anger suppression at three assessment points: before and after a metacognitive intervention as well as at a follow-up 6 months later. Mediation models investigating symptom associations at these three timepoints were conducted. Exploratory analyses investigating these associations in individuals presenting high checking-related symptoms (n = 20) and testing the stability of effects beyond controlling for depressive symptoms and medication intake were conducted.

The sense of responsibility did not significantly predict the level of anger suppression. A temporal association between OCD symptoms (as assessed with the self-report measure) and anger suppression could be evidenced, which was stable beyond controlling for depressive symptoms and medication intake. Against the expectations based on cognitive theories, the sense of responsibility did not predict OCD symptoms. No mediating effect of OCD symptoms was found.

In line with cognitive viewpoints, the present study shows that higher OCD symptoms predict higher levels of anger suppression in a longitudinal design, thereby contributing to the suppression of anger. This effect seems to be independent from depressive symptoms and medication intake. The effect of sense of responsibility on OCD symptoms was less clear and could only be found in the subgroup of patients with OCD and checking-related symptoms, who generally presented higher levels of responsibility. Overall, this is the first study demonstrating temporal associations between OCD symptoms and anger suppression. Acknowledging that anger and anger suppression may be a consequence of OCD symptoms and may also affect aspects of psychotherapy, which can ultimately inform future adjustments to psychotherapeutic treatment.

The experience of self-hood in posttraumatic stress disorder (PTSD) is altered cognitively and somatically. Dysfunctional negative cognitions about the self are a central mechanism of PTSD symptomatology and treatment. However, while higher-order brain models of disturbances in self-appraisal (i.e., cognitive processes relating to evaluating the self) have been examined in other psychiatric disorders, it is unclear how normative brain function during self-appraisal is impaired in PTSD.

This paper presents a PRISMA systematic review of functional neuroimaging studies (n = 5), to establish a neurobiological account of how self-appraisal processes are disturbed in PTSD. The review was prospectively registered with PROSPERO (CRD42023450509).

Self-appraisal in PTSD is linked to disrupted activity in core self-processing regions of the Default Mode Network (DMN); and regions involved in cognitive control and emotion regulation, salience and valuation.

Because self-appraisal in PTSD is relatively under-studied, only a small number of studies could be included for review. Cross-study heterogeneity in analytic approaches and trauma-exposure history prohibited a quantitative meta-analysis.

This paper proposes a mechanistic account of how neural dysfunctions may manifest clinically in PTSD and inform targeted selection of appropriate treatment options. We present a research agenda for future work to advance the field.

Marked dysregulation of the human prefrontal cortex (PFC) and anterior cingulate cortex (ACC) characterises a variety of anxiety disorders, and its amelioration is a key feature of treatment success. Overall treatment response, however, is highly variable, and about a third of patients are resistant to treatment. In this review we hypothesise that a major contributor to this variation in treatment response are the multiple faces of anxiety induced by distinct forms of frontal cortex dysregulation. Comparison of findings from humans and non-human primates reveals marked similarity in the functional organisation of threat regulation across the frontal lobes. This organisation is discussed in relation to the 'predatory imminence continuum' model of threat and the differential engagement of executive functions at the core of both emotion generation and regulation strategies.

This review synthesises individual differences in neural processes related to emotion regulation (ER). It comprises individual differences in self-reported and physiological regulation success, self-reported ER-related traits, and demographic variables, to assess their correlation with brain activation during ER tasks. Considering region-of-interest (ROI) and whole-brain analyses, the review incorporated data from 52 functional magnetic resonance imaging studies. Results can be summarized as follows: (1) Self-reported regulation success (assessed by emotional state ratings after regulation) and self-reported ER-related traits (assessed by questionnaires) correlated with brain activity in the lateral prefrontal cortex. (2) Amygdala activation correlated with ER-related traits only in ROI analyses, while it was associated with regulation success in whole-brain analyses. (3) For demographic and physiological measures, there was no systematic overlap in effects reported across studies. In showing that individual differences in regulation success and ER-related traits can be traced back to differences in the neural activity of brain regions associated with emotional reactivity (amygdala) and cognitive control (lateral prefrontal cortex), our findings can inform prospective personalised intervention models.

Society asks individuals, such as front-line medical and emergency personnel or social media moderators, to help others under highly negative emotional circumstances, and those individuals need to regulate their emotions for their own well being. A well-studied form of emotion regulation is reappraisal, the use of cognitive processes used to reinterpret initial emotional responses to negative events. Distancing (pretending that a situation is distant in time or space) is well documented to be an effective form of emotion regulation, but it may not be applicable in social contexts where individuals must engage with distressing events to help others. Here, for the first time, we asked whether a novel reappraisal strategy focused on Social Good-imagining that an aversive event is also an opportunity to prevent harm to others-can be an effective form of reappraisal. In a pre-registered experiment, participants were randomly assigned to Distancing or Social Good conditions as they viewed neutral or highly aversive images and then reported their subjective emotional states with or without reappraisal. Both Distancing and Social Good reappraisals led to significantly less negative affect. Distancing yielded a stronger effect, but importantly, participants reported both Distancing and Social Good as equally easy to employ and both were effective across multiple demographic and personality characteristics, indicating the broad value of both as effective forms of reappraisal. Across both reappraisal conditions, effective reappraisal increased with age and positive affect. These findings indicate that Social Good is an effective reappraisal strategy and raise the possibility that it could be particularly valuable in contexts in which emotionally demanding tasks are completed on behalf of the good for other people.

Emotion regulation (ER) often is impaired in current or remitted major depression (MD), although the extent of the deficits is not fully understood. Recent studies suggest that frontal alpha asymmetry (FAA) could be a promising electrophysiological measure to investigate ER. The purpose of this study was to investigate ER differences between participants with lifetime major depression (lifetime MD) and healthy controls (HC) for the first time in an experimental task by using FAA. We compared lifetime MD (n = 34) and HC (n = 25) participants aged 18-24 years in (a) an active ER condition, in which participants were instructed to reappraise negative images and (b) a condition in which they attended to the images while an EEG was recorded. We also report FAA results from an independent sample of adolescents with current MD (n = 36) and HC adolescents (n = 38). In the main sample, both groups were able to decrease self-reported negative affect in response to negative images through ER, without significant group differences. We found no differences between groups or conditions in FAA, which was replicated within the independent adolescent sample. The lifetime MD group also reported less adaptive ER in daily life and higher difficulty of ER during the task. The lack of differences between in self-reported affect and FAA between lifetime MD and HC groups in the active ER task indicates that lifetime MD participants show no impairments when instructed to apply an adaptive ER strategy. Implications for interventional aspects are discussed.

The ability to respond to emotional events in a context-sensitive and goal-oriented manner is essential for adaptive functioning. In models of behavioral and emotion regulation, the lateral prefrontal cortex (LPFC) is postulated to maintain goal-relevant representations that promote cognitive control, an idea rarely tested with causal inference. Here, we altered mid-LPFC function in healthy individuals using a putatively inhibitory brain stimulation protocol (continuous theta burst; cTBS), followed by fMRI scanning. Participants performed the Affective Go/No-Go task, which requires goal-oriented action during affective processing. We targeted mid-LPFC (vs. a Control site) based on the individualized location of action-goal representations observed during the task. cTBS to mid-LPFC reduced action-goal representations in mid-LPFC and impaired goal-oriented action, particularly during processing of negative emotional cues. During negative-cue processing, cTBS to mid-LPFC reduced functional coupling between mid-LPFC and nodes of the default mode network, including frontopolar cortex-a region thought to modulate LPFC control signals according to internal states. Collectively, these results indicate that mid-LPFC goal-relevant representations play a causal role in governing context-sensitive cognitive control during emotional processing.

Cognitive reappraisal is an essential emotion regulation skill for social life and psychological health. However, individuals with major depressive disorder (MDD) cannot use this skill effectively. Successful cognitive reappraisal in healthy controls (HC) has been shown to be associated with theta activity in a frontal and subcortical network. In the present study, we investigated whether MDD patients are characterized by altered theta power and connectivity pattern during cognitive reappraisal compared to HC.

Using EEG and eLORETA, we examined both theta activity and connectivity when 25 controls and 24 patients with MDD were asked to complete the emotion cognitive reappraisal task of viewing neutral and negative pictures and reappraise negative pictures. Habitual use of emotion regulation skills was collected using the Cognitive Emotion Regulation Questionnaire (CERQ).

The results showed that MDD patients had (1) reduced theta activity in the left dorsolateral (dlPFC), dorsomedial prefrontal (dmPFC), and rostral-ventral cingulate cortices (rvACC), as well as (2) reduced dlPFC-rvACC theta connectivity than HC during reappraisal. In addition, left dlPFC-rvACC theta connectivity was positively correlated with self-reported cognitive reappraisal in HC. This relation was not observed in MDD. In contrast, CERQ revealed significantly greater use of inadequate regulations skills and significantly lower use of adaptive skills in MDD.

Sample size, limited solution space to cortical grey matter excluding regions such as the amygdala.

This study may indicate a putative frontocingulate dysfunction leading either to an increased use of inadequate emotion regulation or a decreased use of skills that serve to boost positive emotion.

Limited understanding exists regarding the neurobiological mechanisms underlying non-suicidal self-injury (NSSI) and suicide attempts (SA) in depressed adolescents. The maturation of brain network is crucial during adolescence, yet the abnormal alternations in depressed adolescents with NSSI or NSSI+SA remain poorly understood.

Resting-state functional magnetic resonance imaging data were collected from 114 depressed adolescents, classified into three groups: clinical control (non-self-harm), NSSI only, and NSSI+SA based on self-harm history. The alternations of resting-state functional connectivity (RSFC) were identified through support vector machine-based classification.

Convergent alterations in NSSI and NSSI+SA predominantly centered on the inter-network RSFC between the Limbic network and the three core neurocognitive networks (SalVAttn, Control, and Default networks). Divergent alterations in the NSSI+SA group primarily focused on the Visual, Limbic, and Subcortical networks. Additionally, the severity of depressive symptoms only showed a significant correlation with altered RSFCs between Limbic and DorsAttn or Visual networks, strengthening the fact that increased depression severity alone does not fully explain observed FC alternations in the NSSI+SA group.

Convergent alterations suggest a shared neurobiological mechanism along the self-destructiveness continuum. Divergent alterations may indicate biomarkers differentiating risk for SA, informing neurobiologically guided interventions.

The capacity to understand the others' emotional states, particularly if negative (e.g. sadness or fear), underpins the empathic and social brain. Patients who cannot express their emotional states experience social isolation and loneliness, exacerbating distress. We investigated the feasibility of detecting non-invasive scalp-recorded electrophysiological signals that correspond to recalled emotional states of sadness, fear, and joy for potential classification.

The neural activation patterns of 20 healthy and right-handed participants were studied using an electrophysiological technique. Analyses were focused on the N400 component of Event-related potentials (ERPs) recorded during silent recall of subjective emotional states; Standardized weighted Low-resolution Electro-magnetic Tomography (swLORETA) was employed for source reconstruction. The study classified individual patterns of brain activation linked to the recollection of three distinct emotional states into seven regions of interest (ROIs).

Statistical analysis (ANOVA) of the individual magnitude values revealed the existence of a common emotional circuit, as well as distinct brain areas that were specifically active during recalled sad, happy and fearful states. In particular, the right temporal and left superior frontal areas were more active for sadness, the left limbic region for fear, and the right orbitofrontal cortex for happy affective states.

In conclusion, this study successfully demonstrated the feasibility of detecting scalp-recorded electrophysiological signals corresponding to internal and subjective affective states. These findings contribute to our understanding of the emotional brain, and have potential applications for future BCI classification and identification of emotional states in LIS patients who may be unable to express their emotions, thus helping to alleviate social isolation and sense of loneliness.

The widely acknowledged cognitive theory of depression, developed by Aaron Beck, focused on biased information processing that emphasizes the negative aspects of affective and conceptual information. Current attempts to discover the neurological mechanism underlying such cognitive and affective bias have successfully identified various brain regions associated with severally biased functions such as emotion, attention, rumination, and inhibition control. However, the neurobiological mechanisms of how individuals in depression develop this selective processing toward negative is still under question. This paper introduces a neurological framework centered around the frontal-limbic circuit, specifically analyzing and synthesizing the activity and functional connectivity within the amygdala, hippocampus, and medial prefrontal cortex. Firstly, a possible explanation of how the positive feedback loop contributes to the persistent hyperactivity of the amygdala in depression at an automatic level is established. Building upon this, two hypotheses are presented: hypothesis 1 revolves around the bidirectional amygdalohippocampal projection facilitating the amplification of negative emotions and memories while concurrently contributing to the impediment of the retrieval of opposing information in the hippocampus attractor network. Hypothesis 2 highlights the involvement of the ventromedial prefrontal cortex in the establishment of a negative cognitive framework through the generalization of conceptual and emotional information in conjunction with the amygdala and hippocampus. The primary objective of this study is to improve and complement existing pathological models of depression, pushing the frontiers of current understanding in neuroscience of affective disorders, and eventually contributing to successful recovery from the debilitating affective disorders.

Although highly effective on average, exposure-based treatments do not work equally well for all patients with anxiety disorders. The identification of pre-treatment response-predicting patient characteristics may enable patient stratification. Preliminary research highlights the relevance of inhibitory fronto-limbic networks as such. We aimed to identify pre-treatment neural signatures differing between exposure treatment responders and non-responders in spider phobia and to validate results through rigorous replication. Data of a bi-centric intervention study comprised clinical phenotyping and pre-treatment resting-state functional connectivity (rsFC) data of n = 79 patients with spider phobia (discovery sample) and n = 69 patients (replication sample). RsFC data analyses were accomplished using the Matlab-based CONN-toolbox with harmonized analyses protocols at both sites. Treatment response was defined by a reduction of >30% symptom severity from pre- to post-treatment (Spider Phobia Questionnaire Score, primary outcome). Secondary outcome was defined by a reduction of >50% in a Behavioral Avoidance Test (BAT). Mean within-session fear reduction functioned as a process measure for exposure. Compared to non-responders and pre-treatment, results in the discovery sample seemed to indicate that responders exhibited stronger negative connectivity between frontal and limbic structures and were characterized by heightened connectivity between the amygdala and ventral visual pathway regions. Patients exhibiting high within-session fear reduction showed stronger excitatory connectivity within the prefrontal cortex than patients with low within-session fear reduction. Whereas these results could be replicated by another team using the same data (cross-team replication), cross-site replication of the discovery sample findings in the independent replication sample was unsuccessful. Results seem to support negative fronto-limbic connectivity as promising ingredient to enhance response rates in specific phobia but lack sufficient replication. Further research is needed to obtain a valid basis for clinical decision-making and the development of individually tailored treatment options. Notably, future studies should regularly include replication approaches in their protocols.

Many studies have shown that exposure to life events can have a negative impact on mental health. Life events like the death of a spouse or the birth of a child pose a challenge and require temporal or permanent adjustments. Meta-analyses on brain stress responses found bilateral anterior insula activation in response to acute stress. Fear conditioning is assumed a crucial mechanism for the development of anxiety disorders associated with increased activation in the bilateral amygdala. Empirical evidence is lacking regarding the relationship of exposure to recent life events and past childhood adversity with neural processing during fear conditioning.

In the present study, we analyzed data from 103 young, healthy participants. Multiple linear regressions were performed on functional magnetic resonance imaging activation during fear conditioning with the Life Events Scale for Students and the Childhood Trauma questionnaire included as covariates in two separate models.

We found a positive relationship between the number of life events in the last year and left amygdala activation to the conditioned stimulus. A second finding was a positive relationship between childhood adversity and right anterior insula response to the unconditioned stimulus.

Many studies have shown increased amygdala activity after stressful life events. In addition, the anterior insula is activated during acute stress. The present study points to stressor-induced increased salience processing during fear conditioning. We suggest that this could be a potential mechanism for resilience versus mental illness.

Depressed individuals tend to use maladaptive emotion regulation strategies more frequently than non-depressed individuals while using adaptive strategies (e.g., reappraisal) less frequently. Objective neural markers of emotion regulation ability could aid in identifying youth at greatest risk for depression and functional impairment more broadly. We used electroencephalography to examine emotion regulation in adolescents (aged 14-17; N = 201) with current depression (n = 94) and without any history of depression (n = 107) at high (n = 54) and low (n = 53) risk for depression based on a maternal history of depression. Results revealed group differences in event-related potential markers of emotion regulation using multiple scoring approaches. Never-depressed adolescents had significant reductions in mean-activity and principal component analysis-identified late positive potential responses to dysphoric stimuli under reappraisal instructions compared to passive viewing. There was no significant difference in neural responses between conditions among depressed adolescents. The magnitude of the reappraisal effects appeared slightly stronger for low-risk adolescents relative to high-risk. Exploratory analyses further demonstrated that the association between neural markers of emotion regulation and overall functioning was moderated by age, such that impaired emotion regulation abilities predicted poorer functioning among older adolescents. Findings support the sensitivity of the late positive potential to emotion regulation impairments in depression and psychopathology more broadly.

Anxiety and depression co-occur; the neural substrates of shared and unique components of these symptoms are not understood. Given emotional alterations in internalizing disorders, we hypothesized that function of regions associated with emotion processing/regulation, including the anterior cingulate cortex (ACC), amygdala and fusiform gyrus (FG), would differentiate these symptoms. Forty-three adults with depression completed an emotional functional magnetic resonance imaging task and the Hamilton Depression and Anxiety Scales. We transformed these scales to examine two orthogonal components, one representing internalizing symptom severity and the other the type of internalizing symptoms (anxiety vs depression). We extracted blood oxygen level dependent signal from FG subregions, ACC, and amygdala and performed generalized psychophysiological interaction analyses to assess relationships between symptoms and brain function. Type of internalizing symptoms was associated with FG3-FG1 coupling (F = 8.14, P = 0.007). More coupling was associated with a higher concentration of depression, demonstrating that intra-fusiform coupling is differentially associated with internalizing symptom type (anxiety vs depression). We found an interaction between task condition and internalizing symptoms and dorsal (F = 4.51, P = 0.014) and rostral ACC activity (F = 4.27, P = 0.012). Post hoc comparisons revealed that less activity was associated with greater symptom severity during emotional regulation. Functional coupling differences during emotional processing are associated with depressive relative to anxiety symptoms and internalizing symptom severity. These findings could inform future treatments for depression.

A large body of literature suggests that the primary (high callousness-unemotional traits [CU] and low anxiety) and secondary (high CU traits and anxiety) variants of psychopathy significantly differ in terms of their clinical profiles. However, little is known about their neurobiological differences. While few studies showed that variants differ in brain activity during fear processing, it remains unknown whether they also show atypical functioning in motivational and reward system. Latent Profile Analysis (LPA) was conducted on a large sample of adolescents (n = 1416) to identify variants based on their levels of callousness and anxiety. Seed-to-voxel connectivity analysis was subsequently performed on resting-state fMRI data to compare connectivity patterns of the nucleus accumbens across subgroups. LPA failed to identify the primary variant when using total score of CU traits. Using a family-wise cluster correction, groups did not differ on functional connectivity. However, at an uncorrected threshold the secondary variant showed distinct functional connectivity between the nucleus accumbens and posterior insula, lateral orbitofrontal cortex, supplementary motor area, and parietal regions. Secondary LPA analysis using only the callousness subscale successfully distinguish both variants. Group differences replicated results of deficits in functional connectivity between the nucleus accumbens and posterior insula and supplementary motor area, but additionally showed effect in the superior temporal gyrus which was specific to the primary variant. The current study supports the importance of examining the neurobiological markers across subgroups of adolescents at risk for conduct problems to precise our understanding of this heterogeneous population.

Panic disorder (PD) involves emotion dysregulation, but its underlying mechanisms remain poorly understood. Previous research suggests that implicit emotion regulation may play a central role in PD-related emotion dysregulation and symptom maintenance. However, there is a lack of studies exploring the neural mechanisms of implicit emotion regulation in PD using neurophysiological indicators.

To study the neural mechanisms of implicit emotion regulation in PD with event-related potentials (ERP).

A total of 25 PD patients and 20 healthy controls (HC) underwent clinical eva-luations. The study utilized a case-control design with random sampling, selecting participants for the case group from March to December 2018. Participants performed an affect labeling task, using affect labeling as the experimental condition and gender labeling as the control condition. ERP and behavioral data were recorded to compare the late positive potential (LPP) within and between the groups.

Both PD and HC groups showed longer reaction times and decreased accuracy under the affect labeling. In the HC group, late LPP amplitudes exhibited a dynamic pattern of initial increase followed by decrease. Importantly, a significant group × condition interaction effect was observed. Simple effect analysis revealed a reduction in the differences of late LPP amplitudes between the affect labeling and gender labeling conditions in the PD group compared to the HC group. Furthermore, among PD patients under the affect labeling, the late LPP was negatively correlated with disease severity, symptom frequency, and intensity.

PD patients demonstrate abnormalities in implicit emotion regulation, hampering their ability to mobilize cognitive resources for downregulating negative emotions. The late LPP amplitude in response to affect labeling may serve as a potentially valuable clinical indicator of PD severity.

High variability in response and retention rates for posttraumatic stress disorder (PTSD) treatment highlights the need to identify "personalized" or "precision" medicine factors that can inform optimal intervention selection before an individual commences treatment. In secondary analyses from a non-inferiority randomized controlled trial, behavioral and physiological emotion regulation were examined as non-specific predictors (that identify which individuals are more likely to respond to treatment, regardless of treatment type) and treatment moderators (that identify which treatment works best for whom) of PTSD outcome.

There were 85 US Veterans with clinically significant PTSD symptoms randomized to 6 weeks of either cognitive processing therapy (CPT; n = 44) or a breathing-based yoga practice (Sudarshan kriya yoga; SKY; n = 41). Baseline self-reported emotion regulation (Difficulties in Emotion Regulation Scale) and heart rate variability (HRV) were assessed prior to treatment, and self-reported PTSD symptoms were assessed at baseline, end-of-treatment, 1-month follow-up, and 1-year follow-up.

Greater baseline deficit in self-reported emotional awareness (similar to alexithymia) predicted better overall PTSD improvement in both the short- and long-term, following either CPT or SKY. High self-reported levels of emotional response non-acceptance were associated with better PTSD treatment response with CPT than with SKY. However, all significant HRV indices were stronger moderators than all self-reported emotion regulation scales, both in the short- and long-term. Veterans with lower baseline HRV had better PTSD treatment response with SKY, whereas Veterans with higher or average-to-high baseline HRV had better PTSD treatment response with CPT.

To our knowledge, this is the first study to examine both self-reported emotion regulation and HRV, within the same study, as both non-specific predictors and moderators of PTSD treatment outcome. Veterans with poorer autonomic regulation prior to treatment had better PTSD outcome with a yoga-based intervention, whereas those with better autonomic regulation did better with a trauma-focused psychological therapy. Findings show potential for the use of HRV in clinical practice to personalize PTSD treatment.

ClinicalTrials.gov identifier, NCT02366403.

The authors investigated cortico-striatal reactivity to drug cues (as compared with neutral and food cues), drug cue reappraisal, food cue savoring, and their correlations with heroin craving in individuals with heroin use disorder compared with healthy control subjects.

Cross-sectional changes in functional MRI blood-oxygen-level-dependent signal during a novel cue reactivity task were assessed in 32 individuals with heroin use disorder (mean age, 40.3 years; seven women) and 21 age- and sex-matched healthy control subjects (mean age, 40.6 years; eight women).

Drug cue reactivity (vs. neutral cues) was significantly higher in the nucleus accumbens in the heroin use disorder group compared with the control group and nominally significantly higher in the orbitofrontal cortex (OFC); ventromedial prefrontal cortex (vmPFC) activity positively correlated with drug craving. Drug cue reactivity (vs. salient food cues) was also higher in the inferior frontal gyrus (IFG) in the heroin use disorder group compared with the control group. Drug reappraisal and food savoring (vs. passive viewing) showed increased IFG and supplementary motor area activity in all participants; in the heroin use disorder group, higher IFG/dorsolateral PFC (dlPFC) activity during drug reappraisal and rostral anterior cingulate cortex (ACC) activity during food savoring were associated with lower drug cue-induced craving and longer treatment, respectively. A direct comparison of regulation of reactivity to both salient cues revealed widespread group differences such that drug reappraisal activity was higher in the heroin use disorder group and food savoring activity was higher in the control group in both cortical (e.g., OFC, IFG, ACC, vmPFC, and insula) and subcortical (e.g., dorsal striatum and hippocampus) regions. Higher drug reappraisal versus food savoring in the dlPFC was associated with higher self-reported methadone dosage in the heroin use disorder group.

The results demonstrate cortico-striatal upregulation during drug cue exposure and impaired reactivity during processing of alternative non-drug rewards in the heroin use disorder group. Normalizing cortico-striatal function by reducing drug cue reactivity and enhancing natural reward valuation may inform therapeutic mechanisms for reducing drug craving and seeking in heroin addiction.

Emotional experience is central to a fulfilling life. Although exposure to negative experiences is inevitable, an individual's emotion regulation response may buffer against psychopathology. Identification of neural activation patterns associated with emotion regulation via an fMRI task is a promising and non-invasive means of furthering our understanding of the how the brain engages with negative experiences. Prior work has applied multivariate pattern analysis to identify signatures of response to negative emotion-inducing images; we adapt these techniques to establish novel neural signatures associated with conscious efforts to modulate emotional response. We model voxel-level activation via LASSO principal components regression and linear discriminant analysis to predict if a subject was engaged in emotion regulation and to identify brain regions which define this emotion regulation signature. We train our models using 82 participants and evaluate them on a holdout sample of 40 participants, demonstrating an accuracy up to 82.5% across three classes. Our results suggest that emotion regulation produces a unique signature that is differentiable from passive viewing of negative and neutral imagery.

Cognitive reappraisal is an effective emotion regulation strategy involving prefrontal cortex (PFC) control of the amygdala. Its aberrant functioning is closely associated with panic disorder (PD). However, the resting-state functional connectivity (rsFC) between the PFC, implicated in cognitive reappraisal, and the amygdala in PD has not been studied. Thus, this study aims to investigate the rsFC patterns and their association with cognitive reappraisal and PD. This study involved 51 participants, including 26 untreated patients with PD and 25 healthy controls (HC). We evaluated the habit of cognitive reappraisal assessment and the severity of PD using neuropsychological and clinical measures. Resting-state fMRI was utilized to evaluate the rsFC pattern between the PFC, engaged in cognitive reappraisal, and the amygdala. Mediation analysis was performed to explore the role of this rsFC in the relationship between cognitive reappraisal and PD severity. PD patients showed reduced rsFC between the PFC and the amygdala compared to HC. This weakened rsFC was associated with the severity of PD symptoms. Moreover, cognitive reappraisal was negatively correlated with PD severity, and mediation analysis indicated that the rsFC of the PFC-amygdala played a mediating role in this association. Abnormal PFC-amygdala rsFC may play a pivotal role in PD development and/or manifestation and mediate the association between cognitive reappraisal and PD severity, potentially serving as a clinical indicator for monitoring and intervention.

The anterior cingulate cortex (ACC) and right ventrolateral prefrontal cortex (VLPFC) are thought to have important roles in loneliness (feeling of social isolation/exclusion) experience or regulation and in the pathophysiology of their disturbance in major depressive disorder (MDD). However, the structural abnormalities of these regions and the correlates with loneliness in MDD across the healthy population have not fully been clarified. The study analyzed the link between loneliness and gray matter volumes (GMVs) in the ACC and right VLPFC among 1,005 patients with MDD and 7,247 healthy controls (HCs) using UK Biobank data. Significant reductions in GMV in the right VLPFC were found in MDD males compared to HCs. MDD males also showed a higher association between loneliness and reduced GMVs in the right VLPFC and bilateral ACC than HCs. No such associations were found in MDD females. The findings suggest that loneliness may influence brain structures crucial for emotion experience and regulation, particularly in middle-older aged men with MDD. This highlights the potential adverse effects of loneliness on brain structure in MDD and suggests that social engagement could have a positive impact.

Adolescent major depression (MD) is characterized by deficits in emotion regulation (ER). Little is known about the neurophysiological correlates that are associated with these deficits. Moreover, the additional examination of visual attention during ER would allow a more in-depth understanding of ER deficits but has not yet been applied simultaneously.

N = 33 adolescents with MD and n = 35 healthy controls (HCs) aged 12-18 years performed an ER task during which they either a) down-regulated their negative affective response to negative images via cognitive reappraisal or b) attended the images without changing their affective response. During the task, the Late Positive Potential (LPP), gaze fixations on emotional image aspects, and self-reported affective responses were collected simultaneously.

Compared to HCs, adolescents with MD demonstrated reduced ER success based on self-report but did not differ in LPP amplitudes. Participants in both groups showed increased amplitudes in the middle LPP window when they reappraised negative pictures compared to when they attended them. Only in the HC group, increased LPP amplitudes during reappraisal were paralleled by more positive affective responses.

The applied stimuli were part of picture databases and might therefore have limited self-relevance.

Increased LPP amplitude during ER in both groups might be specific to adolescence and might suggest that ER at this age is challenging and requires a high amount of cognitive resources. These findings provide an important starting point for future interventional studies in youth MD.

By combining transcranial magnetic stimulation (TMS) with electroencephalography, human cortical circuits can be directly interrogated. The resulting electrical trace contains TMS-evoked potential (TEP) components, and it is not known whether the amplitudes of these components are stimulus intensity dependent. We examined this in the left dorsolateral prefrontal cortex in nineteen healthy adult participants and extracted TEP amplitudes for the N40, P60, N120, and P200 components at 110%, 120%, and 130% of resting motor threshold (RMT). To probe plasticity of putative stimulus intensity dose-response relationships, this was repeated after participants received intermittent theta burst stimulation (iTBS; 600 pulses, 80% RMT). The amplitude of the N120 and P200 components exhibited a stimulus intensity dose-response relationship, however the N40 and P60 components did not. After iTBS, the N40 and P60 components continued to exhibit a lack of stimulus intensity dose-dependency, and the P200 dose-response was unchanged. In the N120 component, however, we saw evidence of change within the stimulus intensity dose-dependent relationship characterized by a decrease in absolute peak amplitudes at lower stimulus intensities. These data suggest that TEP components have heterogeneous dose-response relationships, with implications for standardizing and harmonizing methods across experiments. Moreover, the selective modification of the N120 dose-response relationship may provide a novel marker for iTBS plasticity in health and disease.

In recent decades, a substantial volume of work has examined the neural mechanisms of cognitive reappraisal. Distancing and reinterpretation are two frequently used tactics through which reappraisal can be implemented. Theoretical frameworks and prior evidence have suggested that the specific tactic through which one employs reappraisal entails differential neural and psychological mechanisms. Thus, we were motivated to assess the neural mechanisms of this distinction by examining the overlap and differentiation exhibited by the neural correlates of distancing (specifically via objective appraisal) and reinterpretation. We analyzed 32 published functional magnetic resonance imaging (fMRI) studies in healthy adults using multilevel kernel density analysis. Results showed that distancing relative to reinterpretation uniquely recruited right bilateral dorsolateral PFC (DLPFC) and left posterior parietal cortex, previously associated with mentalizing, selective attention and working memory. Reinterpretation relative to distancing uniquely recruited left bilateral ventrolateral PFC (VLPFC), previously associated with response selection and inhibition. Further, distancing relative to reinterpretation was associated with greater prevalence of bilateral amygdala attenuation during reappraisal. Finally, a behavioral meta-analysis showed efficacy for both reappraisal tactics. These results are consistent with prior theoretical models for the functional neural architecture of reappraisal via distancing and reinterpretation and suggest potential future applications in region-of-interest specification and neural network analysis in studies focusing on specific reappraisal tactics.

Late-life depression (LLD) is characterized by differences in resting state functional connectivity within and between intrinsic functional networks. This study examined whether clinical improvement to antidepressant medications is associated with pre-randomization functional connectivity in intrinsic brain networks.

Participants were 95 elders aged 60 years or older with major depressive disorder. After clinical assessments and baseline MRI, participants were randomized to escitalopram or placebo with a two-to-one allocation for 8 weeks. Non-remitting participants subsequently entered an 8-week trial of open-label bupropion. The main clinical outcome was depression severity measured by MADRS. Resting state functional connectivity was measured between a priori key seeds in the default mode (DMN), cognitive control, and limbic networks.

In primary analyses of blinded data, lower post-treatment MADRS score was associated with higher resting connectivity between: (a) posterior cingulate cortex (PCC) and left medial prefrontal cortex; (b) PCC and subgenual anterior cingulate cortex (ACC); (c) right medial PFC and subgenual ACC; (d) right orbitofrontal cortex and left hippocampus. Lower post-treatment MADRS was further associated with lower connectivity between: (e) the right orbitofrontal cortex and left amygdala; and (f) left dorsolateral PFC and left dorsal ACC. Secondary analyses associated mood improvement on escitalopram with anterior DMN hub connectivity. Exploratory analyses of the bupropion open-label trial associated improvement with subgenual ACC, frontal, and amygdala connectivity.

Response to antidepressants in LLD is related to connectivity in the DMN, cognitive control and limbic networks. Future work should focus on clinical markers of network connectivity informing prognosis.

ClinicalTrials.gov NCT02332291.

Emotion regulation is a set of processes responsible for controlling, evaluating and adjusting reactions to achieve a goal. Results derived from magnetic resonance imaging agreed on the involvement of frontal and limbic structures in this process. Findings using cognition and physiology interactions are still scarce but suggest a role of alpha rhythm in emotional induction and for theta in regulation.

Our goal was to investigate alpha and theta rhythm during the reappraisal of aversive stimuli. We hypothesized that an implication of alpha rhythm in emotional induction only and an increase in prefrontal theta rhythm positively correlated with successful regulation.

Twenty-four healthy participants were recorded with 64 EEG electrodes while asked to watch or reappraise negative pictures passively. Theta and alpha rhythms were compared across maintain, decrease and increase regulation conditions, and a source localization estimated the generators.

Theta activity was consistently higher in the upregulation than in the maintenance condition (p = .04) for the entire control period, but mainly at the beginning of regulation (1-3 s) for low-theta and later (5-7 s) for high-theta. Moreover, our results confirm that a low-theta generator correlated with mainly the middle frontal gyrus and the anterior dorsal cingulate cortex during upregulation. Theta was sensitive to emotion upregulation, whereas the alpha oscillation was non-sensitive to emotion induction and regulation.

Theta rhythm was involved explicitly in emotion upregulation processes that occur at a definite time during reappraisal, whereas the alpha rhythm was not altered by emotion induction and regulation.