Empathy relies on distinct but interacting processes for representing others’ states and regulating self-oriented affect. Neuroimaging studies implicate the right temporoparietal junction (rTPJ) in perspective-taking and the left dorsolateral prefrontal cortex (lDLPFC) in emotion regulation, yet causal evidence from neuromodulation remains limited. This study compared the effects of rTPJ- and lDLPFC-targeted transcranial direct current stimulation (tDCS) on empathy across multiple contexts and modalities.

In Study 1, participants performed a static pain empathy task following anodal or sham tDCS over the rTPJ or lDLPFC, with electroencephalography recorded. In Study 2, participants viewed autobiographical videos depicting positive, negative, and neutral events before and after stimulation, while heart rate variability (HRV) was assessed. Machine learning-based decoding integrated behavioral and physiological data to evaluate the ‘readability’ of empathic states.

rTPJ-tDCS enhanced cognitive empathy across tasks, increasing empathic ratings and late positive potential amplitudes in the pain empathy task, and enhancing the subjective sense of content and emotion understanding in the video task. lDLPFC-tDCS selectively increased HRV in the video task, consistent with greater autonomic flexibility, without altering explicit ratings. Decoding analyses converged with these findings: rTPJ stimulation increased classification accuracy of targets’ emotional states, indicating stronger alignment between empathic responses and others’ emotional cues, whereas lDLPFC stimulation reduced accuracy, suggesting regulation-related attenuation of overt emotional signals.

These findings provide causal evidence for rTPJ supporting cross-context cognitive empathy and lDLPFC modulating autonomic regulation. Multi-context, multimodal assessment delineated distinct target-specific profiles, informing precision neuromodulation strategies for empathy-related deficits and regulation needs.

Previous taxometric studies have yielded inconsistent findings regarding the empirical support for the common clinical practice of categorizing patients into discrete suicide risk groups (low versus high risk). Furthermore, potential sex differences in these latent structures have not been adequately explored. This study aimed to investigate the latent structure of suicide risk based on motivational and volitional phase symptoms from the ideation-to-action framework, and to explore potential sex differences in these latent structures, in order to determine whether the clinical practice of categorizing patients into low versus high suicide risk categories is empirically valid.

We employed taxometric procedures to examine whether suicide risk should be understood as dimensional or categorical. Our analysis distinctly evaluated motivational and volitional phase symptoms across separate samples of male and female outpatients with mood disorders.

Our research revealed significant sex differences in the latent structure of suicide risk. For motivational phase symptoms, an ambiguous structure was revealed in the male group, whereas a clearly dimensional latent structure was observed in the female group. For volitional phase symptoms, a categorical structure emerged in males, while a dimensional structure was found in females.

Given the ‘gender paradox’ in suicidal behavior, which highlights higher rates of fatal suicide attempts among males, early identification of the high-volitional-risk group and focused allocation of intervention resources are particularly crucial for males. Our findings underscore the necessity for sex-specific approaches to suicide risk assessments, research applying the ideation-to-action framework, and targeted intervention development.

Systemic inflammation is hypothesized to contribute to post-traumatic stress disorder (PTSD) vulnerability. Few studies have examined inflammation shortly after trauma as a predictor of later PTSD symptoms. We examined whether inflammation from the emergency department (ED) post-trauma is associated with PTSD symptom severity over the following 6 months.

Our sample included 742 AURORA participants, a longitudinal cohort of patients in 29 EDs across the United States after a traumatic stressor, followed up to 6 months. Plasma cytokines were assessed from a study blood draw in the ED: an inflammatory index (standardized sum of generally pro-inflammatory markers interleukin [IL]-6, IL-8, tumor necrosis factor alpha [TNF-α], interferon gamma [IFN-γ]), and generally anti-inflammatory IL-10. PTSD symptoms were self-reported at 2 weeks, 8 weeks, 3 months, and 6 months post-ED. Covariate-adjusted repeated-measures regressions estimated associations between inflammation and PTSD symptoms, overall and sex-stratified.

Among 742 participants (age m = 40.0 [13.7]; 479 [64.6%] female), PTSD symptoms were elevated then modestly decreased over follow-up. Higher ED inflammation was associated with higher PTSD symptoms across follow-up (standardized symptoms β = 0.05, 95% CI: 0.01–0.09), adjusted for potential confounders. Higher pro-inflammatory index levels and IL-6, IL-8, and TNF-α were associated with higher PTSD symptoms in males only, while higher IL-10 was associated with higher PTSD symptoms in females only.

Pro-inflammatory levels shortly after traumatic stress are associated with heightened PTSD symptoms, particularly among males. Inflammatory markers may prove useful additions to prediction models for PTSD following trauma, with attention to sex differences.

In recent decades, the potency of cannabis resin increased globally, raising concerns, as higher potency has been associated with increased risk of psychiatric harms at the individual level. The aim here was to examine whether changes over time in the potency of seized cannabis resin samples were associated with psychiatric harms at the population level.

Data on ∆-9-tetrahydrocannabinol (THC) concentration in seized cannabis resin were obtained from forensic departments in Denmark (2000–2022), the country reporting the highest potency in Europe. Data on admissions to cannabis treatment, incidence of cannabis-induced psychosis, and dual diagnosis (schizophrenia and cannabis use disorder) were obtained from national registers. Time-dependent associations between potency and the outcomes were examined with mixed-effects linear regression models and associations across age and sex were explored. Candidate time lags were 0–10 years.

THC concentration increased almost fourfold: mean 8.3–31.2% from 2000 to 2022. In fully adjusted models, THC was positively associated with first-time cannabis treatment entry at lags of 0–6, strongest at year 0 (p < 0.0001); incidence of cannabis-induced psychosis at lags of 0–4, strongest at year 0 (p < 0.0001); and incidence of dual diagnosis at lags of 0–1, strongest at year 0 (p < 0.01). No positive associations were found in unadjusted models. Subgroup analyses indicated associations in older patients and women.

Potency of seized cannabis resin increased almost fourfold from 2000 to 2022. Changes in cannabis potency were positively associated with psychiatric harms at the population level across all outcomes.

Predicting suicide risk remains a challenge. We examined whether neurocognitive performance on implicit associations toward suicide, motor speed, response inhibition, and executive functioning predicts suicide attempt and behavior in high-risk psychiatric patients.

Our sample (N = 298) consisted of inpatients (n = 161) and outpatients (n = 83) admitted for a suicide attempt (SA; n = 78), for suicidal ideation (SI; n = 76), or were non-suicidal psychiatric controls (PC; n = 90), and healthy controls (HC; n = 54). Participants were followed for 12 months, with follow-up assessments at 3-, 6-, and 12-months. Neurocognitive tasks were administered at baseline. Clinical symptom measures, suicidality, and electronic health record data were collected at each timepoint. ANCOVA was used to compare groups on neurocognitive performance, and logistic and Cox regressions examined whether neurocognitive performance predicted future actual suicide attempt and suicidal behaviors.

Participants had a mean age of 24.34 years (SD = 3.71). A total of 19 participants made an actual suicide attempt during the study. On neurocognitive tasks at baseline, the SA group had stronger implicit associations with death- and suicide-related words compared to the HC (d = 0.88, p < 0.001) and SI (d = 0.63, p = 0.005) groups and poorer executive functioning than the SI (d = 0.44, p = 0.043) group in multivariate models. Stronger implicit associations with death/suicide predicted higher risk of suicide attempts at the univariate (HR = 1.68 p = 000), but not multivariate level (HR = 1.17 p = 000), while slower motor speed predicted actual suicide attempts (HR = 1.81 p = 000) at the multivariate level.

Slower motor speed predicts actual suicide attempt and may help identify psychiatric patients who are at high risk for suicidal behavior.

Existing evidence highlights sleep’s critical role in regulating cortisol stress recovery; the underlying neural pathways remain unclear. To address this gap, the current study aims to elucidate the neurobiological pathway linking objective sleep efficiency to cortisol stress recovery using functional magnetic resonance imaging (fMRI), with a focus on the functional connectivity (FC) between prefrontal cortex (PFC) and hippocampus.

Seventy-seven participants completed an acute stress task during a task-dependent and resting-state fMRI scanning. Salivary samples were collected and analyzed as an indicator of cortisol stress recovery. Objective sleep efficiency was measured the night before the fMRI scanning. Using Seed-based gPPI and resting-state FC analysis, we examined the mediating role of PFC-hippocampus FC in the association between objective sleep efficiency and cortisol stress recovery, both during the stress task and in the post-stress resting-state.

Objective sleep efficiency was significantly related to cortisol stress recovery but not with cortisol reactivity. Neurologically, higher sleep efficiency was linked to enhanced prefrontal activity and increased the left dlPFC-hippocampus FC during the acute stress task. Importantly, objective sleep efficiency promoted cortisol stress recovery by the weakened resting-state left dlPFC-hippocampus FC.

This study highlights the pivotal role of left dlPFC-hippocampus regulation underlying sleep’s effect on HPA axis recovery to acute stress. These results suggest a model whereby high objective sleep efficiency promotes adaptive stress recovery through dynamic reallocation of neural resources across acute stress process, characterized by task-dependent coupling and post-stress decoupling of frontal-hippocampal circuitry.

The duration of untreated psychosis (DUP) is still considerably long in patients with psychotic disorders worldwide. Social determinants, such as the socioeconomic status, can influence DUP, exacerbating health inequalities in access to timely care. We investigated whether subpopulations with shared characteristics are associated with longer DUP.

We performed latent class analyses to investigate whether classes with shared configurations of social and substance use-related risks can be identified in two large cohorts with psychotic disorders: N = 780 patients from the GROUP project and N = 847 patients from the EU-GEI project. Subsequently, we conducted survival analyses to analyze whether identified classes are associated with DUP.

We identified three classes in both samples. Membership of the class with predominantly younger men, higher proportion of cannabis use, and supported living was associated with longer DUP compared with a class with predominantly White ethnicity, higher education, and current employment in GROUP (HR = 1.28, 95% CI: 1.06–1.56, p = .011) and in EU-GEI (HR = 1.27, 95% CI: 1.07–1.51, p = .007). In GROUP, membership of a third class with predominantly White women, without cannabis use, was associated with the shortest DUP (HR = 0.78, 95% CI: 0.63–0.95, p = .016).

Results suggest that specific populations differ in their risk distributions for prolonged DUP and highlight the importance of considering configurations of social determinants in context. Public mental health programs need to establish their differential impact for diverse populations and facilitate more targeted pathways to care.

Methylphenidate is sometimes used to address residual symptoms of major depressive disorder (MDD), but concerns about psychiatric destabilization and limited long-term evidence have constrained its use. We examined the psychiatric safety of methylphenidate in adults with MDD in a large, real-world cohort.

Using the TriNetX Global Collaborative Network, we identified adults with MDD who initiated methylphenidate and matched them 1:1 with controls who did not receive methylphenidate. Patients with attention-deficit/hyperactivity disorder, bipolar disorder, mania, or recent psychiatric destabilization were excluded. The primary outcome was a composite of all-cause hospitalization or emergency room visits; secondary outcomes included hospitalization, emergency visits, suicidal behavior, manic episodes, and recurrence of MDD. Hazard ratios (HRs) were estimated with Cox proportional hazards models after propensity score matching.

Of 425,190 eligible patients, 3,211 matched pairs were included (mean age, 55.8 years; 58% female). Over 1 year, the composite outcome occurred less frequently in the methylphenidate group than in controls (574 vs. 694; HR, 0.85; 95% CI, 0.76–0.95). No significant differences were observed for hospitalization, emergency visits, suicidal behavior, manic episodes, or MDD recurrence. Results were consistent across subgroups defined by sex, age, and antidepressant class.

In adults with MDD, methylphenidate use was associated with a lower risk of hospitalization or emergency visits and was not linked to increased risk of suicidality, mania, or recurrence. These findings support the psychiatric safety of methylphenidate as an adjunctive treatment for selected patients, though longer follow-up is needed.

Prior neuroimaging studies and meta-analyses investigating brain correlates of placebo analgesia (PA) have yielded neuroanatomically heterogeneous findings, which may be reconciled from a connectomics perspective. The objective of this study was to examine network localization of brain functional alterations related to PA.

We initially identified PA-induced brain activation alterations (hyper-activation and hypo-activation separately) during experimental pain from 29 published studies with 674 individuals. By combining these implicated dysfunctional brain regions with large-scale discovery (N = 1113) and validation (N = 1093) resting-state functional magnetic resonance imaging datasets, we then employed a novel functional connectivity network mapping approach to construct PA hyper-activation and hypo-activation networks, respectively.

The PA hyper-activation network manifested as a pattern of circumscribed brain regions mainly involving the limbic, default, and frontoparietal networks. By contrast, the PA hypo-activation network comprised a broadly distributed set of brain regions primarily implicating the ventral attention, somatomotor, and subcortical networks.

Our findings regarding the brain network representations of PA may contribute to a deeper understanding of its action mechanisms and provide a neural framework that may inform future clinical translation.

Cognitive neuropsychological models propose that antidepressants exert their therapeutic effects by modifying negative emotional processing biases early in treatment. However, evidence from large, long-term clinical samples is limited.

We conducted a mechanistic analysis within the Antidepressants to Prevent Relapse in Depression randomized controlled trial, which compared maintenance antidepressant treatment with placebo substitution in adults with recurrent depression who were currently well (N = 478). Participants completed a computerized facial emotion recognition task at baseline, 12 weeks, and 52 weeks, in which faces morphed from happy to sad. The primary outcome was the number of faces classified as happy (0–45). Linear and longitudinal mixed-effects models were used to compare treatment groups and examine associations with depressive (PHQ-9) and anxiety (GAD-7) symptoms.

Of the 462 participants completing at least one task, there was no evidence that discontinuing antidepressants altered performance compared with maintenance at 12 weeks (adjusted mean difference = 0.23, 95% CI –0.5 to 1.0, p = 0.5) or 52 weeks (0.29, –0.5 to 1.2, p = 0.5). Depressive symptoms were negatively associated with happy face classifications both cross sectionally (β = –0.20 per PHQ-9 point, p = 0.02) and longitudinally (β = –0.09, p = 0.05). Anxiety symptoms were positively associated with happy classifications (β = 0.11, p = 0.047).

Maintenance antidepressant treatment did not sustain positive emotional processing biases as indexed by facial emotion recognition, despite robust associations between such biases and depressive symptoms. These findings challenge the generalizability of laboratory evidence on emotional bias modification to long-term clinical treatment and highlight the need for further mechanistic research on antidepressant action.

Youth mental health and brain development are profoundly shaped by highly heterogeneous childhood environments. However, research often operates under the assumption that neural networks linked to psychopathology function in the same way across different individuals, with limited consideration of how brain-behavior associations themselves may vary across environmental contexts. This poses challenges for identifying the precise neural correlates of risk or resilience to psychopathology.

In a large, longitudinal sample (N = 8,078), we examined differences in psychological symptoms and their associations with brain network functional connectivity across three clusters of youth identified by their home, school, and community environments.

Child environment groups differed in mental health symptoms, as well as the links between large-scale functional network connectivity and symptoms. Youth exposed to high trauma and familial risk showed the highest symptom levels over time compared to those youth in low-risk or economically disadvantaged environments. Moreover, youth in the high trauma and familial risk group showed stronger functional connectivity between the salience and frontoparietal networks with increased symptoms, whereas youth in the high disadvantage group showed the opposite pattern. Notably, these brain and mental health associations were not observed when examined across the entire sample, and group differences were more pronounced in female and older youth.

The same neural patterns of functional network connectivity can have different implications for mental health depending on the environment. These findings highlight the importance of context-sensitive approaches for developing personalized interventions in supporting youth mental health.

Adverse childhood experiences (ACEs) are associated with increased risk of psychotic-like experiences (PLEs), but the relationship between specific adversities and the persistence of PLEs in young people remains unclear. We examined associations between distinct ACEs and the persistence of PLEs until 24 years old.

Using longitudinal data from participants in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort with at least one PLE datapoint, we used group-based trajectory modeling to estimate longitudinal trajectories of PLEs from age 12–24. We examined their associations with bullying victimization, maltreatment, parental mental health problems, parental substance abuse, parental separation, and parental intimate partner violence prior to first PLE experiences.

Among 4,448 participants, a three-group trajectory model provided the best fit, revealing low, increasing and persistent PLE groups from ages 12–24. In fully adjusted multinomial logistic regression models, those exposed to bullying were more likely to belong to either the increasing (relative risk ratio [RRR]: 1.83, 95%CIs: 1.26–2.66) or high (RRR: 1.78, 95%CIs: 1.07–2.93) PLEs group than the low PLE group; those exposed to maltreatment were more likely to be in the increasing PLE group (RRR: 1.47, 95%CIs: 1.03–2.10). No other ACEs were associated with PLE trajectories.

Bullying was associated with persistent PLEs up to 24 years old, independent of other forms of childhood adversity, with timing-specific effects of maltreatment on increasing symptoms emerging later in adolescence. Findings provide further evidence for the importance of prioritizing bullying and maltreatment reduction as public health targets.

Insomnia is common in major depressive disorder (MDD), and varying severity of insomnia may be associated with distinct neural alterations in MDD. Dynamic functional connectivity can capture time-varying brain network interactions and may help disentangle insomnia-related mechanisms in MDD.

We recruited 203 drug-naïve adult MDD patients, divided into high- (HI-MDD, n = 133) and low-insomnia (LI-MDD, n = 70) groups using the Hamilton Depression Rating Scale insomnia subscale, along with 122 health controls (HCs). Independent component analysis and a sliding-window approach were applied to explore static and dynamic functional network connectivity (FNC).

While static FNC revealed no significant group difference, dynamic analysis identified distinct connectivity states between two groups. Compared to HCs, HI-MDD displayed more frequent occurrence of state I and less of state IV, a pattern was absent in LI-MDD. Both MDD groups showed increased default mode network (DMN)-lateral ventral attention network (VAN) connectivity in states I and II, accompanied by decreased dorsal attention network-cerebellar/DMN connectivity in state I relative to HCs. Compared with LI-MDD, HI-MDD exhibited enhanced DMN-medial VAN connectivity in state II, along with increased DMN connectivity with visual and sensorimotor networks in state I, suggesting insomnia-related changes. In addition, we identified insomnia-related memory deficits and depression-related processing speed impairment in MDD. Insomnia significantly moderated the association between altered DMN-lateral VAN connectivity in state I and logical memory impairment in MDD.

These findings suggest that insomnia severity in MDD is associated with distinct temporal patterns of brain network alterations beyond shared depression-related changes and moderate cognitive functions in MDD.

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental condition with widespread brain structure alterations. However, the relationship between macroscale cortical organization and microscale molecular mechanisms remains unclear, particularly regarding the neurobiological mechanisms shared between the full ADHD cohort and its combined subtype (ADHD-C).

We analyzed 176 patients with ADHD (105 ADHD-C, 71 ADHD inattentive subtype) and 176 matched typically developing (TD) controls from the ADHD-200 dataset. Morphometric Inverse Divergence (MIND) networks quantified cortical similarity. Partial least squares (PLS) regression linked case–control MIND differences to cortical gene expression, assessing functional enrichment, cell-type specificity, and developmental trajectories.

Neuroanatomically, the ADHD-C subtype exhibited widespread increases in regional MIND values, particularly in temporal and parietal cortices, reflecting greater inter-regional morphological homogeneity. PLS regression revealed that these MIND alterations were spatially correlated with a specific transcriptomic signature (PLS1+). These PLS1+ genes were significantly enriched in mitochondria-related metabolic pathways and showed distinct cortical layer specificity (notably layer V) and developmental stage specificity (from late fetal to late infancy stages). Regarding cell-type specificity, while PLS1+ genes in the full ADHD cohort were significantly enriched in excitatory and inhibitory neurons, the ADHD-C subtype showed similar but trend-level associations. Importantly, the full ADHD cohort and the ADHD-C group shared numerous PLS1-related genes and broad functional pathway enrichment commonalities.

This study links macroscale cortical abnormalities to microscale transcriptional regulation, with pronounced alterations in ADHD-C. The shared genetic and functional profiles between ADHD and its combined subtype underscore common pathological processes, providing novel insights into the neurodevelopmental mechanisms of ADHD.

Intrusive trauma memories – vivid, distressing recollections that occur involuntarily and may feel present – is a defining symptom of post-traumatic stress disorder (PTSD). While traditional models emphasize dysregulation within limbic-prefrontal circuits, emerging evidence implicates visual sensory systems in the formation of trauma-memory intrusions. However, direct causal evidence remains lacking.

We combined functional MRI with repetitive transcranial magnetic stimulation (rTMS) to examine the causal role of visual sensory cortices in intrusive memory formation. Healthy participants underwent a trauma-film paradigm, followed by fMRI scanning during memory encoding and a post-encoding resting phase during which spontaneous intrusions were recorded. One group received 1-Hz rTMS targeting early visual cortex (V1/V2); a control group received stimulation at the Vertex. Intrusive memories were recorded over the subsequent 7 days.

rTMS to V1/V2 significantly reduced the frequency, vividness, and emotional intensity of intrusive memories, while preserving recognition of episodic gist. fMRI analyses showed that intrusive episodes were associated with heightened activation and stable neural representations within the occipital visual cortex (OVC). Functional and effective connectivity analyses further revealed that the occurrence of intrusions was predicted by interactions between the middle frontal gyrus (MFG) and OVC. Dynamic causal modeling confirmed direct, bidirectional MFG-OVC interactions that coexisted with, but tracked the intrusion dynamics more closely than, the traditional prefrontal-limbic circuits.

These findings provide the first causal evidence for the direct involvement of the early visual cortex in trauma-memory intrusions. They highlight the visual system as a novel neuromodulation target for therapeutic intervention on PTSD.

Psychotic experiences (PEs) in are associated with elevated risk for mental health difficulties. This study examined predictors of PEs, inclusive of the role of gender, ethnicity, and protective factors.

Data were drawn from a 2021 Planet Youth survey of adolescents (n = 4,005). PEs were measured using the adolescent psychotic symptom screener. Effects of psychosocial predictors on PEs were measured by fitting multivariable logistic regression main effect and joint exposure models.

29.8% reported PEs. Black/Asian/Other minorities had elevated odds (aOR = 1.59, 95% CI 1.26–2.02, p < .001). Increased odds in males, females, undisclosed gender and non-binary/transgender with elevated emotional/behavioural difficulties (aOR = 4.47, 95% CI 3.53–5.67, p < .001; aOR = 3.25, 95% CI 2.59–4.08, p < .001; aOR = 4.83, 95% CI 2.58–9.02, p < .001; aOR = 4.33, 95% CI 2.69–6.97, p < .001 respectively). High odds in undisclosed gender with low emotional/behavioural difficulties (aOR = 4.36, 95% CI 1.50–12.66, p = .007). Lower odds from perceived school/home safety (aOR = 0.69, 95% CI 0.58–0.83, p < .001 and (aOR = 0.81, 95% CI 0.66–0.99, p = .038, respectively). Elevated odds from recent adversities (aOR = 1.91, 95% CI 1.47–2.49, p = .011) attenuated by parental support (aOR = 1.76, 95% CI 1.17–2.65, p < .001). Each additional adversity (>12 months) increased odds (aOR = 1.12, 95% CI 1.07–1.17, p < .001).

Findings highlight the interplay of risk and protective factors in adolescent PEs, with increased vulnerability among minoritized youth. Results support targeted interventions to reduce mental health disparities.

Gambling disorder (GD) involves persistent risky choices despite losses, suggesting impaired impulse control. While static paradigms reveal inhibition deficits in GD, they cannot model dynamic risk-reward escalations during real gambling. This study aims to investigate whether GD involves impaired dynamic impulse control during escalating stakes and to dissociate contributions of subjective risk evaluation and trait impulsivity to this deficit.

Using a sequential gambling task with 83 male patients with GD and 62 matched healthy controls (HCs), this study investigated dynamic impulse control deficits under escalating stakes. We quantified dynamic impulse control via the reward–reaction time (RT) coupling for ‘continue’ choices (dynamic impulse control index [DICI]) using Bayesian modeling. Risk sensitivity and risk preference were derived from stop/continue decisions. Trait impulsivity was assessed with the Barratt Impulsiveness Scale (BIS-11). Regression analyses examined the modulation of DICI by risk sensitivity and trait impulsivity.

Patients with GD exhibited significantly attenuated DICI versus HCs, reflecting failure to increase deliberation with escalating stakes. Computational modeling revealed markedly reduced risk sensitivity in GD despite comparable risk preference. Critically, trait impulsivity positively modulated DICI in HCs but not in GD, indicating pathological decoupling. Risk sensitivity positively predicted DICI in both groups, though significantly weaker in GD.

These findings establish a triadic impairment in GD: (1) attenuated adaptive impulse control during escalation (impaired DICI), (2) deficient subjective risk weighting (reduced sensitivity), and (3) breakdown of impulsivity-based modulation of control. This reveals a dynamic, mechanism-focused pathology beyond static trait models.