Prenatal maternal stress is a known risk factor for later emotional problems, yet not all exposed offspring develop psychopathology. Executive functioning and prefrontal cortex structure and activity may buffer these effects, but it remains unclear whether genetic predispositions in these domains moderate associations with adolescent internalizing symptoms.

We examined 3,111 adolescents (1,881 females, 1,230 males). Prenatal stress was measured via a cumulative index across four domains. Internalizing symptoms were self-reported at ages 14 and 16. Genetic predisposition for executive functioning was indexed using a polygenic score (PGS) derived from adult samples, applied here to estimate genetic predisposition for executive functioning in adolescence. We also estimated a prefrontal cortex PGS based on cortical thickness and activation in six prefrontal regions, with a composite index derived from the first principal axis summarizing these measures.

Higher prenatal stress was significantly associated with more internalizing symptoms in adolescence. Female sex and maternal genetic risk for internalizing symptoms were also associated with higher symptom levels. Neither genetic disposition for executive functioning nor prefrontal cortex moderated this association overall. However, a weak interaction emerged at age 16, indicating that a genetic disposition for higher executive functioning was associated with greater internalizing symptoms under high stress exposure.

Prenatal maternal stress predicted increased adolescent internalizing symptoms, with limited evidence for moderation by genetic predisposition for executive functioning. Higher genetic potential for executive functioning may confer increased sensitivity to early stress under certain developmental conditions.

Gaming disorder (GD) is increasingly recognized for its adverse impact on social functioning, yet the underlying neural mechanisms remain unclear, particularly during real-time social interactions. This study examined neural differences in the prefrontal cortex (PFC) and temporoparietal junction (TPJ) during cooperation and competition tasks in adolescents and young adults with GD.

Using functional near-infrared spectroscopy (fNIRS), we examined 175 male participants, classified into Gaming Disorder (n = 42), Hazardous Gaming (n = 69), and Healthy Control (n = 64) groups. Participants performed cooperation and competition tasks while activation, functional connectivity, and network topology were assessed within the PFC and TPJ.

In the current study, GD participants exhibited significantly greater impairments in social and emotional functioning compared to the HG and HC groups. The GD group showed increased right TPJ activation during cooperation and decreased activation during competition. Both GD and HG groups demonstrated heightened medial PFC activation and functional connectivity, indicating compensatory engagement. Graph theory analysis revealed disrupted network topology in GD, including reduced nodal efficiency and centrality within the PFC and TPJ. Neural alterations were significantly correlated with clinical measures, including gaming duration and social-emotional deficits.

This study identifies critical neural disruptions underlying social dysfunction in GD, particularly within mentalizing and executive control networks. The neural markers observed in the GD group have important implications for clinical diagnosis and targeted intervention, whereas similar patterns in the HG group highlight opportunities for early detection and preventive strategies.

Offspring of parents with bipolar disorder (BD offspring) face elevated risks for emotional dysregulation and cognitive deficits, particularly in working memory. This study investigates working memory deficits and their neural correlates in BD offspring.

We assessed 41 BD offspring and 25 age-matched healthy controls (HCs) using a spatial N-back task and task-related functional magnetic resonance imaging (fMRI).

Compared to HCs, BD offspring exhibit reduced accuracy and lower signal-detection sensitivity (d′) on the 1-back task. fMRI reveals hyperactivation in the right intracalcarine cortex/lingual gyrus (ICC/LG) in BD offspring, particularly during the 1-back condition. Psychophysiological interaction (PPI) analyses show reduced connectivity between the right ICC/LG and the left postcentral gyrus in BD offspring as task load increases from 0-back to 1-back. This connectivity positively correlates with 1-back task performance in HCs but not in BD offspring. Additionally, using bilateral dorsolateral prefrontal cortex (DLPFC) as regions of interest, PPI analyses show diminished condition-dependent connectivity between the left DLPFC and the left superior frontal gyrus/paracingulate cortex, and between the right DLPFC and the left postcentral gyrus/precentral gyrus in BD offspring as the task load increases.

These findings suggest that BD offspring exhibit working memory deficits and impaired neural connectivity involving both sensory processing and higher-order cognitive systems. Such deficits may emerge at a genetically predisposed stage of bipolar disorder, underscoring the significance of early identification and intervention strategies.

Neuroimaging studies suggest alterations in prefrontal cortex (PFC) activity in healthy adults under stress. Adolescents with non-suicidal self-injury (NSSI) report difficulties in stress and emotion regulation, which may be dependent on their level of borderline personality disorder (BPD).

The aim was to examine alterations in the PFC in adolescents with NSSI during stress.

Adolescents (13–17 years) engaging in non-suicidal self-injury (n = 30) and matched healthy controls (n = 29) performed a task with low cognitive demand and the Trier Social Stress Test (TSST). Mean PFC oxygenation across the PFC was measured with an eight-channel near-infrared spectroscopy system. Alongside self-reports on affect, dissociation and stress, BPD pathology was assessed via clinical interviews.

Mixed linear-effect models revealed a significant effect of time on PFC oxygenation and a significant time×group interaction, indicating increased PFC activity in patients engaging in NSSI at the beginning of the TSST compared with healthy controls. Greater BPD symptoms overall were associated with an increase in PFC oxygenation during stress. In exploratory analyses, mixed models addressing changes in PFC connectivity over time as a function of BPD symptoms were significant only for the left PFC.

Results indicate differences in the neural stress response in adolescents with NSSI in line with classic neuroimaging findings in adults with BPD. The link between PFC oxygenation and measures of BPD symptoms emphasises the need to further investigate adolescent risk-taking and self-harm across the spectrum of BPD, and maybe overall personality pathology, and could aid in the development of tailored therapeutic interventions.

Divergent thinking is a critical creative cognitive process. Its neural mechanisms have been well-studied through structural and functional imaging in healthy individuals but are less explored in patients with bipolar disorder (BD). Because of the traditional link between creativity and BD, this study investigated the structural correlates of divergent thinking in patients with BD through surface-based morphometry.

Fifty-nine patients diagnosed with BD I or BD II (35.3 ± 8.5 years) and 56 age- and sex-matched controls (33.9 ± 7.4 years) were recruited. The participants underwent structural magnetic resonance imaging and an evaluation of divergent thinking by using the Chinese version of the Abbreviated Torrance Test for Adults (ATTA). FreeSurfer 7.0 was used to generate thickness and surface area maps for each participant. Brainwise regression of the association between cortical thickness or surface area and ATTA performance was conducted using general linear models.

Divergent thinking performance did not differ significantly between the patients with BD and the healthy controls. In these patients, total ATTA score was negatively correlated with cortical thickness in the right middle frontal gyrus, right occipital, and left precuneus but positively correlated with the surface area of the right superior frontal gyrus. By contrast, total ATTA scores and cortical thickness or surface area were not significantly correlated among the controls.

The findings indicate that divergent thinking involves cerebral structures for executive control, mental imagery, and visual processing in patients with BD, and the right prefrontal cortex might be the most crucial of these structures.

Borderline personality disorder (BPD) is a severe psychiatric disorder conceptualised as a disorder of emotion regulation. Emotion regulation has been linked to a frontolimbic network comprising the dorsolateral prefrontal cortex and the amygdala, which apparently synchronises its activity via oscillatory coupling in the theta frequency range.

To analyse whether there are distinct differences in theta oscillatory coupling in frontal brain regions between individuals with BPD and matched controls during emotion regulation by cognitive reappraisal.

Electroencephalogram (EEG) recordings were performed in 25 women diagnosed with BPD and 25 matched controls during a cognitive reappraisal task in which participants were instructed to downregulate negative emotions evoked by aversive visual stimuli. Between- and within-group time–frequency analyses were conducted to analyse regulation-associated theta activity (3.5–8.5 Hz).

Oscillatory theta activity differed between the participants with BPD and matched controls during cognitive reappraisal. Regulation-associated theta increases were lower in frontal regions in the BPD cohort compared with matched controls. Functional connectivity analysis for regulation-associated changes in the theta frequency band revealed a lower multivariate interaction measure (MIM) increase in frontal brain regions in persons with BPD compared with matched controls.

Our findings support the notion of alterations in a frontal theta network in BPD, which may be underlying core symptoms of the disorder such as deficits in emotion regulation. The results add to the growing body of evidence for altered oscillatory brain dynamics in psychiatric populations, which might be investigated as individualised treatment targets using non-invasive stimulation methods.

Catatonia is a psychomotor syndrome frequently observed in disorders with neurodevelopmental impairments, including psychiatric disorders such as schizophrenia. The orbitofrontal cortex (OFC) has been repeatedly associated with catatonia. It presents with an important interindividual morphological variability, with three distinct H-shaped sulcal patterns, types I, II, and III, based on the continuity of the medial and lateral orbital sulci. Types II and III have been identified as neurodevelopmental risk factors for schizophrenia. The sulcal pattern of the OFC has never been investigated in catatonia despite the role of the OFC in the pathophysiology and the neurodevelopmental component of catatonia.

In this context, we performed a retrospective analysis of the OFC sulcal pattern in carefully selected homogeneous and matched subgroups of schizophrenia patients with catatonia (N = 58) or without catatonia (N = 65), and healthy controls (N = 82).

Logistic regression analyses revealed a group effect on OFC sulcal pattern in the left (χ2 = 18.1; p < .001) and right (χ2 = 28.3; p < .001) hemispheres. Catatonia patients were found to have more type III and less type I in both hemispheres compared to healthy controls and more type III on the left hemisphere compared to schizophrenia patients without catatonia.

Because the sulcal patterns are indirect markers of early brain development, our findings support a neurodevelopmental origin of catatonia and may shed light on the pathophysiology of this syndrome.