Compulsive cleaning is a characteristic symptom of a particular subtype of obsessive–compulsive disorder (OCD) and is often accompanied by intense disgust. While overgeneralization of threat is a key factor in the development of obsessive–compulsive symptoms, previous studies have primarily focused on fear generalization and have rarely examined disgust generalization. A systematic determination of the behavioral and neural mechanisms underlying disgust generalization in individuals with contamination concern is crucial for enhancing our understanding of OCD.

In this study, we recruited 27 individuals with high contamination concerns and 30 individuals with low contamination concerns. Both groups performed a disgust generalization task while undergoing functional magnetic resonance imaging (fMRI).

The results revealed that individuals with high contamination concern had higher disgust expectancy scores for the generalization stimulus GS4 (the stimulus most similar to CS+) and exhibited higher levels of activation in the left insula and left putamen. Moreover, the activation of the left insula and putamen were positively correlated with a questionnaire core of the ratings of disgust and also positively correlated with the expectancy rating of CS+ during the generalization stage.

Hyperactivation of the insula and putamen during disgust generalization neutrally mediates the higher degree of disgust generalization in subclinical OCD individuals. This study indicates that altered disgust generalization plays an important role in individuals with high contamination concerns and provides evidence of the neural mechanisms involved. These insights may serve as a basis for further exploration of the pathogenesis of OCD in the future.

Because pediatric anxiety disorders precede the onset of many other problems, successful prediction of response to the first-line treatment, cognitive-behavioral therapy (CBT), could have a major impact. This study evaluates whether structural and resting-state functional magnetic resonance imaging can predict post-CBT anxiety symptoms.

Two datasets were studied: (A) one consisted of n = 54 subjects with an anxiety diagnosis, who received 12 weeks of CBT, and (B) one consisted of n = 15 subjects treated for 8 weeks. Connectome predictive modeling (CPM) was used to predict treatment response, as assessed with the PARS. The main analysis included network edges positively correlated with treatment outcome and age, sex, and baseline anxiety severity as predictors. Results from alternative models and analyses are also presented. Model assessments utilized 1000 bootstraps, resulting in a 95% CI for R2, r, and mean absolute error (MAE).

The main model showed a MAE of approximately 3.5 (95% CI: [3.1–3.8]) points, an R2 of 0.08 [−0.14–0.26], and an r of 0.38 [0.24–0.511]. When testing this model in the left-out sample (B), the results were similar, with an MAE of 3.4 [2.8–4.7], R2−0.65 [−2.29–0.16], and r of 0.4 [0.24–0.54]. The anatomical metrics showed a similar pattern, where models rendered overall low R2.

The analysis showed that models based on earlier promising results failed to predict clinical outcomes. Despite the small sample size, this study does not support the extensive use of CPM to predict outcomes in pediatric anxiety.

Depression has been linked to disruptions in resting-state networks (RSNs). However, inconsistent findings on RSN disruptions, with variations in reported connectivity within and between RSNs, complicate the understanding of the neurobiological mechanisms underlying depression.

A systematic literature search of PubMed and Web of Science identified studies that employed resting-state functional magnetic resonance imaging (fMRI) to explore RSN changes in depression. Studies using seed-based functional connectivity analysis or independent component analysis were included, and coordinate-based meta-analyses were performed to evaluate alterations in RSN connectivity both within and between networks.

A total of 58 studies were included, comprising 2321 patients with depression and 2197 healthy controls. The meta-analysis revealed significant alterations in RSN connectivity, both within and between networks, in patients with depression compared with healthy controls. Specifically, within-network changes included both increased and decreased connectivity in the default mode network (DMN) and increased connectivity in the frontoparietal network (FPN). Between-network findings showed increased DMN–FPN and limbic network (LN)–DMN connectivity, decreased DMN–somatomotor network and LN–FPN connectivity, and varied ventral attention network (VAN)–dorsal attentional network (DAN) connectivity. Additionally, a positive correlation was found between illness duration and increased connectivity between the VAN and DAN.

These findings not only provide a comprehensive characterization of RSN disruptions in depression but also enhance our understanding of the neurobiological mechanisms underlying depression.

According to the aberrant salience proposal, reward processing abnormality, specifically erroneous reward prediction error (RPE) signaling due to stimulus-independent release of dopamine, underlies delusions in schizophrenia. However, no studies to date have examined RPE-associated brain activations in relation to this symptom.

Seventy-eight patients with a DSM-5 diagnosis of schizophrenia/schizoaffective disorder and 43 healthy individuals underwent fMRI while they performed a probabilistic monetary reward task designed to generate a measure of RPE. Ratings of delusions and referentiality were made in the patients.

Using whole-brain, voxel-based analysis, schizophrenia patients showed only minor differences in RPE-associated activation compared to healthy controls. Within the patient group, however, severity of delusions was inversely associated with RPE-associated activation in areas including the caudate nucleus, the thalamus and the left pallidum, as well as the lateral frontal cortex bilaterally, the pre- and postcentral gyrus and supplementary motor area, the middle cingulate gyrus, and parts of the temporal and parietal cortex. A broadly similar pattern of association was seen for referentiality.

According to this study, while patients with schizophrenia as a group do not show marked alterations in RPE signaling, delusions and referentiality are associated with reduced activation in parts of the prefrontal cortex and the basal ganglia, though not specifically the ventral striatum. The direction of the changes is on the face of it contrary to that predicted by aberrant salience theory.

Maternal perinatal mental health is essential for optimal brain development and mental health of the offspring. We evaluated whether maternal depression during the perinatal period and early life of the offspring might be selectively associated with altered brain function during emotion regulation and whether those may further correlate with physiological responses and the typical use of emotion regulation strategies.

Participants included 163 young adults (49% female, 28–30 years) from the ELSPAC prenatal birth cohort who took part in its neuroimaging follow-up and had complete mental health data from the perinatal period and early life. Maternal depressive symptoms were measured mid-pregnancy, 2 weeks, 6 months, and 18 months after birth. Regulation of negative affect was studied using functional magnetic resonance imaging, concurrent skin conductance response (SCR) and heart rate variability (HRV), and assessment of typical emotion regulation strategy.

Maternal depression 2 weeks after birth interacted with sex and showed a relationship with greater brain response during emotion regulation in a right frontal cluster in women. Moreover, this brain response mediated the relationship between greater maternal depression 2 weeks after birth and greater suppression of emotions in young adult women (ab = 0.11, SE = 0.05, 95% CI [0.016; 0.226]). The altered brain response during emotion regulation and the typical emotion regulation strategy were also as sociated with SCR and HRV.

These findings suggest that maternal depression 2 weeks after birth predisposes female offspring to maladaptive emotion regulation skills and particularly to emotion suppression in young adulthood.

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.

Maternal depression is associated with difficulties in understanding and adequately responding to children’s emotional signals. Consequently, the interaction between mother and child is often disturbed. However, little is known about the neural correlates of these parenting difficulties. Motivated by increasing evidence of the amygdala’s important role in mediating maternal behavior, we investigated amygdala responses to child sad and happy faces in mothers with remitted major depression disorder (rMDD) relative to healthy controls.

We used the sensitivity subscale of the emotional availability scales and functional magnetic resonance imaging in 61 rMDD and 27 healthy mothers to examine the effect of maternal sensitivity on mothers’ amygdala responses to their children’s affective facial expressions.

For mothers with rMDD relative to controls, we observed decreased maternal sensitivity when interacting with their child. They also showed reduced amygdala responses to child affective faces that were associated with lower maternal sensitivity. Connectivity analysis revealed that this blunted amygdala response in rMDD mothers was functionally correlated with reduced activation in higher-order medial prefrontal areas.

Our results contribute toward a better understanding of the detrimental effects of lifetime depression on maternal sensitivity and associated brain responses. By targeting region-specific neural activation patterns, these results are a first step toward improving the prediction, prevention, and treatment of depression-related negative effects on mother–child interaction.

Anxiety symptoms are elevated among people with joint hypermobility. The underlying neural mechanisms are attributed theoretically to effects of variant connective tissue on the precision of interoceptive representations contributing to emotions.

To investigate the neural correlates of anxiety and hypermobility using functional neuroimaging.

We used functional magnetic resonance neuroimaging to quantify regional brain responses to emotional stimuli (facial expressions) in people with generalised anxiety disorder (GAD) (N = 30) and a non-anxious comparison group (N = 33). All participants were assessed for joint laxity and were classified (using Brighton Criteria) for the presence and absence of hypermobility syndrome (HMS: now considered hypermobility spectrum disorder).

Participants with HMS showed attenuated neural reactivity to emotional faces in specific frontal (inferior frontal gyrus, pre-supplementary motor area), midline (anterior mid and posterior cingulate cortices) and parietal (precuneus and supramarginal gyrus) regions. Notably, interaction between HMS and anxiety was expressed in reactivity of the left amygdala (a region implicated in threat processing) and mid insula (primary interoceptive cortex) where activity was amplified in people with HMS with GAD. Severity of hypermobility in anxious, compared with non-anxious, individuals correlated with activity within the anterior insula (implicated as the neural substrate linking anxious feelings to physiological state). Amygdala-precuneus functional connectivity was stronger in participants with HMS, compared with non-HMS participants.

The predisposition to anxiety in people with variant connective tissue reflects dynamic interactions between neural centres processing threat (amygdala) and representing bodily state (insular and parietal cortices). Correspondingly, interventions to regulate amygdala reactivity while enhancing interoceptive precision may have therapeutic benefit for symptomatic hypermobile individuals.

Psychostimulants and nonstimulants have partially overlapping pharmacological targets on attention-deficit/hyperactivity disorder (ADHD), but whether their neuroimaging underpinnings differ is elusive. We aimed to identify overlapping and medication-specific brain functional mechanisms of psychostimulants and nonstimulants on ADHD.

After a systematic literature search and database construction, the imputed maps of separate and pooled neuropharmacological mechanisms were meta-analyzed by Seed-based d Mapping toolbox, followed by large-scale network analysis to uncover potential coactivation patterns and meta-regression analysis to examine the modulatory effects of age and sex.

Twenty-eight whole-brain task-based functional MRI studies (396 cases in the medication group and 459 cases in the control group) were included. Possible normalization effects of stimulant and nonstimulant administration converged on increased activation patterns of the left supplementary motor area (Z = 1.21, p < 0.0001, central executive network). Stimulants, relative to nonstimulants, increased brain activations in the left amygdala (Z = 1.30, p = 0.0006), middle cingulate gyrus (Z = 1.22, p = 0.0008), and superior frontal gyrus (Z = 1.27, p = 0.0006), which are within the ventral attention network. Neurodevelopmental trajectories emerged in activation patterns of the right supplementary motor area and left amygdala, with the left amygdala also presenting a sex-related difference.

Convergence in the left supplementary motor area may delineate novel therapeutic targets for effective interventions, and distinct neural substrates could account for different therapeutic responses to stimulants and nonstimulants.