BACKGROUND:Although Attention-Deficit/Hyperactivity Disorder (ADHD) is characterized by complex inhibitory deficits, generalized interventions often show poor patient engagement and adherence. This study compared domain-specific inhibitory control in children and adolescents with ADHD to characterize the precise nature of these deficits. METHODS:A cross-sectional comparative design was used with 146 participants, comprising 82 children (aged 9-11) and 64 adolescents (aged 16-18), including both ADHD and typically developing groups. Participants completed three computerized paradigms targeting distinct inhibitory subdomains: The Stroop Color-Word Test (interference control), the Cued Go/No-Go Task (proactive and reactive control; action restraint), and the Stop-Signal Task (reactive inhibition, action cancellation). RESULTS:A significant neurocognitive dissociation emerged. Interference control (Stroop performance) was selectively preserved in the ADHD group: latency did not differ from TD peers, but response accuracy under interference was significantly reduced. In contrast, youth with ADHD showed pronounced reactive inhibition deficits on both the Cued Go/No-Go and Stop-Signal tasks, reflected in significantly slower reaction times and longer Stop-Signal Reaction Times. As a supplementary finding, proactive inhibitory control did not differ between groups, indicating relatively preserved proactive control in ADHD. Significant main effects of group and age emerged for most inhibitory control measures, with no significant Group × Age interactions. CONCLUSIONS:The selective impairment of reactive inhibition (both action restraint and action cancellation), together with selectively preserved (latency-based but not accuracy-based) interference control, challenges the utility of "one-size-fits-all" cognitive training. The comparatively spared proactive inhibition further supports a domain-specific, rather than global, account of inhibitory dysfunction in ADHD. These findings underscore the need for targeted, process- and parameter-specific intervention approaches that precisely target motor inhibition rather than broad attentional filtering.
BACKGROUND:The available metacognition scales have not been translated in the Indian population. AIM:This study aimed to translate the Metacognition Self-Assessment Scale (MSAS) and the Metacognition Questionnaire (MCQ-30) into Hindi and to evaluate the internal consistency and split-half reliability of the Hindi versions. Additional objectives were to compare the metacognitive impairments among schizophrenia patients and healthy controls. METHODOLOGY:MSAS and MCQ-30 were translated into Hindi using the World Health Organisation guidelines, and the Hindi versions were administered to 100 schizophrenia patients and 117 healthy controls enrolled through convenience sampling. RESULTS:The Cronbach's alpha of MSAS was 0.949 and 0.899 for the schizophrenia and control groups, respectively. The Cronbach's alpha of MCQ-30 was 0.9 and 0.826, for the schizophrenia and control groups, respectively. Patients with schizophrenia performed poorly on MSAS when compared to healthy controls. However, on MCQ-30, both groups were comparable. CONCLUSIONS:The present study also suggests that patients with schizophrenia perform poorly on MSAS when compared to healthy controls. However, on MCQ-30, both groups are comparable in metacognition functioning.
BACKGROUND:Dopaminergic dysregulation has been implicated in the pathophysiology of bipolar disorder (BD), yet how state-dependent alterations in presynaptic dopaminergic markers relate to large-scale brain networks remains unclear. We aimed to examine longitudinal, within-subject associations between striatal dopamine transporter (DAT) availability and functional connectivity (FC) across mood states in BD. METHODS:Outpatients with BD underwent repeated neuroimaging during euthymic and depressive states. Striatal DAT availability was measured using ^99mTc-TRODAT-1 single-photon emission computed tomography, and resting-state functional magnetic resonance imaging was used to assess striatal seed-based FC. Paired t tests compared DAT availability across mood states. General linear and linear mixed models examined DAT-FC associations and DAT-mood interactions, adjusting for age and sex. RESULTS:Thirty-three patients were enrolled. Within-individual analyses showed lower bilateral dorsal-striatal DAT availability during depression than euthymia. During euthymia, DAT availability was associated with stronger dorsal striatum connectivity with the dorsal and middle cingulate regions, whereas during depression it was negatively associated with connectivity to the precuneus. Linear mixed models showed mood-dependent associations of dorsal-striatal DAT availability with connectivity involving the precuneus, insula, and supramarginal gyrus. Reduced dorsal striatum-ACC and supramarginal connectivity during depression was associated with greater depressive symptom severity. CONCLUSION:Striatal DAT availability and cortico-striatal functional connectivity showed coordinated, state-dependent changes in BD. These findings provide evidence for state-dependent associations between presynaptic dopaminergic markers and large-scale functional networks in BD.
BACKGROUND:General self-efficacy (GSE) is an influential transdiagnostic determinant of resilience and psychological vulnerability. Although several abbreviated versions of the General Self-Efficacy Scale (GSES) exist, their ability to reproduce the classification structure of the GSES remains unclear. METHODS:This cross-sectional study used two-step cluster analyses to classify community-dwelling adults with and without acquired movement disabilities (N = 120; 50% females) according to the GSES and its shortened forms. Classification agreement was assessed using Cohen's kappa. Criterion validity was examined by associating clustering variables with life satisfaction and health locus of control. RESULTS:The seven-item and Skliarova's six-item versions displayed poor agreement (κ = 0.291, p < .001). Romppel's six-item as well as five-item, and three-item versions demonstrated moderate-to-excellent agreement with the GSES (κ = 0.662-0.827; p < .001). Both full and abbreviated models identified balanced high-, moderate-, and low-GSE profiles. Lower GSE profile was associated with longer disability duration and singleness, whereas higher GSE profile was linked to younger age and shorter disability duration. Significant between-cluster differences emerged for life satisfaction and internal health locus of control (p-values ≤.011). CONCLUSIONS:The shortened GSES retains its profiling capacity. Reduced GSE is associated with poorer wellbeing among those with longer disability histories and singleness, highlighting potential targets for psychosocial interventions.
BACKGROUND:Familial vulnerability and environmental adversity are both associated with adolescent substance-use, yet their joint effects remain insufficiently characterized. This study examined their interaction using a latent gene-environment (GxE) framework in the cVEDA cohort. METHODS:The sample included 3786 adolescents and young adults aged 12-24 years. Familial vulnerability was indexed as the family-history density (FHD) scores derived from the pedigree for medical and psychiatric conditions, adjusted for degree of relatedness. Environmental adversity was captured using measures of childhood adversity, school climate, and parenting experiences. Substance use summarized as a global continuum of risk score from the WHO ASSIST. Weighted latent G×E models were estimated using an alternating optimization approach, adjusting for age and sex. Competing susceptibility patterns were compared, and predictive performance was evaluated using five-fold cross validation. RESULTS:Familial vulnerability and environmental adversity were each associated with greater substance use involvement, with evidence that familial vulnerability amplified environmental effects. The latent familial composite was driven primarily by family history of alcohol dependence (ηp2=0.03) and other psychiatric disorders (ηp2=0.044). The latent environmental composite was dominated by adverse childhood experiences (ηp2=0.042) and unsafe school climate (ηp2=0.029), with smaller contributions from childhood neglect and negative parenting practices (ηp2<0.01). Model comparisons suggested a weak differential susceptibility pattern. Cross validation showed good discrimination (AUC=0.84). CONCLUSIONS:Youth with greater familial vulnerability appear more environmentally sensitive, consistent with a "for-better-and-for-worse" pattern typical of differential susceptibility model. Integrating family risk screening with interventions targeting school climate, childhood adversity, and parenting may help identify targets for substance use prevention.
