This study aimed to explore the correlates of zero, one, and multiple performance validity test (PVT) failures on cognitive test performance in patients with various degrees of severity of traumatic brain injury.

306 participants completed the Trail Making Test as part of a neuropsychological evaluation within 1–36 months post-injury. They were assigned to zero, one, or ≥ two fail groups on the basis of at least two independent PVTs. Group differences in Trail Making Test performance were analyzed with analysis of variance, with post hoc contrasts with the Bonferroni correction for multiple comparisons. Groups were also compared on various background characteristics.

Participants who passed all PVTs had statistically significantly better performance on both parts of the Trail Making Test as compared to those who failed either one or multiple PVTs, with the latter two groups not differing statistically significantly from each other. PVT failure was relatively more common in participants who were female, had an uncomplicated mild TBI, were involved in financial compensation-seeking, and were seen at a longer time point since injury.

Failure of even only one PVT is associated with lower neuropsychological test performance in patients with traumatic brain injury, especially when empirically validated criteria are used that are stratified by injury severity. Such failure does not always reflect malingering but must be interpreted and addressed in the context of patient background characteristics.

Language deficits are frequently described by patients with multiple sclerosis (MS); however, objective characterization remains somewhat limited due to its omission from standard MS cognitive evaluation and the inconsistent findings that arise from current language measures.

To establish alternative approaches to characterizing single-word level language in MS, this study (i) validates the Sydney Language Battery (SYDBAT) visual confrontation naming subtest and (ii) examines the insights provided by examining naming errors and latencies.

40 MS patients from Royal Melbourne Hospital’s Cognitive Neuroimmunology Clinic and 40 matched controls completed a series of neuropsychological tests, including the SYDBAT and ‘gold standard’ confrontation naming task, the Boston Naming Test (BNT). Error types and latencies on the SYDBAT were extracted from assessment audio recordings.

SYDBAT and BNT scores were highly correlated (r = 0.81, p < .001) and these tasks reported comparable receiver operating characteristic curves (p = .091). Latency analysis captured lexical retrieval difficulties, with patients displaying significantly longer mean latencies than controls on the SYDBAT (p = .012, β = 0.54).

These findings support the validity of the SYDBAT and value of the latency analysis in characterizing language impairment in MS. Use of the SYDBAT and latency considerations contribute to a broader assessment with a briefer administration time compared to gold-standard evaluation. The study thereby offers clinicians an enhanced toolkit to more effectively and appropriately evaluate language functioning and supplement standard cognitive evaluation in this population.

To compare verbal memory encoding, storage, and retrieval in patients with schizophrenia (SZ), SZ plus substance use disorder (SZ+), and substance use disorder only (SUD), testing the hypothesis that SZ + group exhibits greater impairment across all processes.

A total of 294 male patients under treatment (SZ = 72, SZ+ = 72, SUD = 150) meeting DSM-5 criteria completed the Rey Auditory Verbal Learning Test (RAVLT). RAVLT measures assessed encoding, storage, and retrieval. ANCOVA/MANCOVA, controlling for premorbid IQ, were used to explore group differences.

Significant differences among groups were observed in all RAVLT measures (F(2,291) > 9.25, p < 0.001, ηp2 > 0.06) except retrieval. Post hoc analyses revealed that both SZ and SZ+ groups showed significant verbal memory impairments (learning trials and storage, interference, short and long-term recall and recognition) compared to the SUD group which performed within the normative range. The SZ and SZ+ groups showed altered values (Z ≥ −1.5) from the second learning trial onward and total learning, and the SZ+ group also for long-term recall and recognition.

This study confirms the existence of significant verbal memory deficits in both SZ and SZ+ groups compared to SUD. Verbal memory impairment appears as a central feature of SZ spectrum disorders, irrespective of SUD comorbidity. Exacerbated memory impairment in SZ+ compared to SZ on the RAVLT is subtle without reaching significant differences, although consideration of altered Z-scores suggests worse performance in SZ+ in encoding and consolidation processes. Further research should explore clinical variables and moderators of comorbidity effects in SZ.

Clinical progression during psychosis has been closely associated with grey matter abnormalities resulting from atypical brain development. However, the complex interplay between psychopathology and heterogeneous maturational trajectories challenges the identification of neuroanatomical features that anticipate symptomatic decline.

To investigate cortical volume longitudinal deviations in first-episode psychosis (FEP) using normative modelling, exploring their relationship with long-term cognitive and symptomatic outcomes, as well as their cytoarchitectural and neurobiological underpinnings.

We collected magnetic resonance imaging (MRI), cognitive and symptomatic data from 195 healthy controls and 357 drug-naïve or minimally medicated FEP individuals that were followed up 1, 3, 5 and 10 years following the first episode (1209 MRI scans and assessments in total). Using normative modelling, we derived subject-specific centile scores for cortical volume to investigate atypical deviations in FEP and their relationship to long-term cognitive and symptomatic deterioration. The resulting centile association maps were further characterised by examining their cytoarchitectural and neurobiological attributes using normative atlases.

FEP centiles demonstrated a widespread reduction at treatment initiation, with longitudinal analysis showing an increase during treatment time, indicating convergence towards normal maturation trajectories. Interestingly, this effect was reduced in highly medicated individuals. Additionally, we found that cognitive impairments experienced during early FEP stages worsened under long-term medication. Positive symptomatology was negatively associated with regional centiles, and individuals with higher centiles benefited most from treatment. Cytoarchitectural and neurobiological analyses revealed that regional centiles related to FEP, as well as to symptomatology, were associated with specific molecular features, such as regional serotonin and dopamine receptor densities.

Collectively, these findings underscore the potential use of centile-based normative modelling for a better understanding of how atypical cortical development contributes to the long-term clinical progression of neurodevelopmental conditions.

To extend the current understanding of executive function (EF) deficits in youth with neurofibromatosis type 1 by investigating the impact of cognitive load on performance compared to typically developing children.

In this prospective multicenter study, 42 children with neurofibromatosis type 1 (NF1) (ages 7–18) completed neuropsychological assessments of intellect and executive functioning. Age- and sex-matched controls (n = 42) were drawn from the normative database for the tasks of executive control (TEC). Multivariate and supplementary univariate analyses examined group differences and task effects (inhibitory control and working memory demand). Associations between TEC performance and parent-reported executive dysfunction (BRIEF) were also explored.

Both groups showed reduced accuracy and speed with increased inhibitory demand and made fewer errors with increased working memory demand. However, children with NF1 were significantly less accurate and consistent across tasks, particularly under higher cognitive load, while controls improved or maintained performance. Significant group × cognitive load interactions were observed, and laboratory-based deficits in NF1 were associated with parent-reported executive dysfunction.

Children with NF1 experience unique and multidimensional decrements in EF performance in response to increased cognitive load, unlike typically developing peers. These deficits appear to be clinically relevant. Targeting working memory and inhibitory control may reduce susceptibility to cognitive overload and improve outcomes for children with NF1.

One of the challenges of psychological research is obtaining a sample representative of the general population. One largely overlooked participant characteristic is sub-clinical levels of psychiatric symptoms.

A series of studies were conducted to assess (i) whether typical psychology study participants had more psychiatric symptoms than the general population, (ii) whether there are sub-groups defined by psychiatric symptoms within the no-diagnosis, no-medication participant pool, and (iii) whether sub-clinical levels of psychiatric symptoms have an effect on standard behavioral tasks. Five UK national datasets (N > 10,000) were compared to data from psychology study participants (Study 1: n = 872; Study 2: n = 43,094; Study 3: n = 267).

Psychology study participants showed significantly higher levels of anxiety and depression and lower well-being, according to four commonly used mental health measures (GHQ-12, PHQ-8, WEMWBS, and WHO-5). Five sub-groups within the psychology study participant group were identified based on symptom levels, ranging from none to significant psychiatric symptoms. These groupings predicted performance on tests of executive function, including the Stroop task and the n-back task, as well as measures of intelligence.

This study demonstrates that standard psychology participant pools are unrepresentative and suggests that a failure to account for psychiatric symptoms when recruiting for any psychological study is likely to negatively impact the reproducibility and generalizability of psychological science.

Most children recover from mild traumatic brain injury (mTBI), but some experience persistent neurocognitive effects. Understanding is limited due to methodological differences and a lack of pre-injury data. The study aimed to assess changes in neurocognitive outcomes in children following mTBI compared to orthopedic injury (OI) and non-injured (NI) controls, while accounting for pre-injury functioning.

Data were drawn from the Adolescent Brain and Cognitive Development (ABCD) study, a prospective longitudinal cohort. The sample included children with mTBI between the 1-year and 2-year follow-ups (n = 83), identified by parent report of head injury with memory loss or loss of consciousness, compared to children who experienced OI within the same period (n = 231) and an NI control group (n = 218). Changes in neurocognitive outcomes from baseline to the 2-year follow-up between groups (mTBI vs. OI; mTBI vs. NI) were estimated using linear mixed-effects models, accounting for demographic, behavioral, genetic, and white matter microstructural covariates.

At baseline prior to injury, the mTBI group demonstrated better performance on picture vocabulary and crystallized composite scores than the OI group. At post-injury, after adjusting for pre-injury baseline differences, children who sustained an mTBI were no different in any measure of neurocognitive outcomes compared to OI and NI controls.

The findings highlight the importance of accounting for pre-injury differences when evaluating neurocognitive outcomes following pediatric mTBI. Neurocognitive differences within a year post-injury may be more related to pre-existing individual factors rather than the injury itself, underscoring the need for a comprehensive approach in studying pediatric mTBI.

Major depressive disorder (MDD) is a heterogeneous with underlying mechanisms that are insufficiently studied. We aimed to identify functional connectivity (FC)-based subtypes of MDD and investigate their biological mechanisms.

Consensus clustering of FC patterns was applied to a population of 829 MDD patients from the REST-Meta-MDD database, with validity assessed across multiple dimensions, including atlas replication, cross-validated classification, and drug-naïve subgroup analysis. Regression models were used to quantify FC alterations in each MDD subgroup compared with 770 healthy controls, and to analyze spatial associations between FC alterations and publicly available gene transcriptomic and neurotransmitter receptor/transporter density databases.

Two stable MDD subtypes emerged: hypoconnectivity (n = 527) and hyperconnectivity (n = 299), which had both shared and distinct regions with remarkable FC alterations (i.e. epicenters) in the default mode network.

There were several common enriched genes (e.g. axon/brain development, synaptic transmission/organization, etc.) related to FC alterations in both subtypes. However, glial cell and neuronal differentiation genes were specifically enriched in the hypoconnectivity and hyperconnectivity subtypes, respectively.

Both subtypes showed spatial associations between FC alterations and serotonin receptor/transporter density. In the hypoconnectivity subtype, FC alterations correlated with GABA and acetylcholine receptor densities, while norepinephrine transporter and glutamate receptor densities were linked to the hyperconnectivity subtype.

Our findings suggested the presence of two neuroimaging subtypes of MDD characterized by hypoconnectivity or hyperconnectivity, demonstrating robust reproducibility. The two subtypes had both shared and distinct genetic mechanisms and neurotransmitter receptor/transporter profiles, suggesting potential clinical implications for this heterogeneous disorder.

To investigate potential contributors to mental fatigue after aneurysmal subarachnoid hemorrhage (aSAH) and angiographically negative subarachnoid hemorrhage (anSAH), with a focus on information processing speed, attentional control, and psychological distress.

This observational study included 101 patients (70 aSAH, 31 anSAH) and 86 controls. Neuropsychological assessments and questionnaires were conducted five months post-SAH. Mental and physical fatigue were assessed with the Dutch Multifactor Fatigue Scale, information processing speed and attentional control with the Trail Making Test and Vienna Test System Reaction Time and Determination Test, and psychological distress with the Hospital Anxiety and Depression Scale.

Patients reported significantly higher mental and physical fatigue than controls (p < .001) and information processing speed and attentional control were significantly lower (p < .05), with no differences between aSAH and anSAH groups. Severe mental fatigue was present in 55.7% of patients with aSAH and 61.3% of patients with anSAH, significantly exceeding the prevalence of severe physical fatigue (p < .05). Higher mental fatigue correlated with worse attentional control in aSAH and with lower information processing speed in anSAH. Both mental and physical fatigue correlated with psychological distress, particularly after anSAH.

The factors related to mental fatigue appear to differ based on the type of SAH, potentially involving problems in information processing speed and attentional control, psychological distress, or both. This study emphasizes the need for individualized rehabilitation strategies addressing both cognitive and psychological factors in managing mental fatigue after SAH.

Negative symptoms in schizophrenia, particularly motivational deficits, pose significant challenges to treatment and recovery. Despite their profound impact on functional outcomes, these symptoms remain poorly understood and inadequately addressed by current interventions.

The CHANSS (Characterising Negative Symptoms in Schizophrenia) study aims to dissect the cognitive mechanisms underlying motivational impairments by focusing on three interconnected domains: executive cognition, motivational cognition and meta-cognition.

This large, international, cross-sectional study recruits a heterogeneous sample of patients across illness stages – from first-episode psychosis to treatment-resistant schizophrenia – and uses a comprehensive cognitive battery, clinical scales, self-report measures and computerised cognitive tasks. Four novel tasks assess key processes in motivated behaviour: option generation, reward-based decision-making, risk sensitivity and performance self-evaluation. By incorporating control for secondary influences like depression, psychosis, sedation and illness chronicity, the study seeks to identify distinct cognitive and behavioural subtypes within motivational dysfunction.

CHANSS tests the hypothesis that specific patient profiles exhibit predominant impairments in one or more cognitive domains, which may differentially affect goal-directed behaviour. The study’s design allows exploration of hierarchical relationships between cognitive processes, such as how neurocognitive deficits may cascade to impair motivation and self-evaluation.

Ultimately, CHANSS aims to advance mechanistic understanding of motivational deficits in schizophrenia and pave the way for personalised, targeted interventions. Its findings may inform future clinical trials and contribute to a shift away from one-size-fits-all approaches towards more effective, stratified treatment strategies in schizophrenia.

While prior studies have analyzed Skin Picking Disorder as a unitary condition, little research has been done examining clinical and neurocognitive characteristics of specific subtypes. The objective of this study is to analyze differences in impulsivity, emotional regulation, symptom severity, cognitive performance, and the presence of comorbid psychiatric conditions between focused and automatic subtypes of Skin Picking Disorder.

83 adults aged 18–65 with skin picking disorder were enrolled at the University of Chicago and separated into 4 skin picking subtype groups based on high or low levels of focused and automatic picking scores on the Milwaukee Inventory for the Dimension of Adult Skin Picking. The 4 subtype groups were separated using K-means clustering. Each group completed the same clinical and neurocognitive assessments. ANOVA or Chi-Squared tests were used to analyze differences in assessment outcomes.

Higher focused picking scores were significantly associated with greater symptom severity and impairment. Differences in levels of automatic/focused picking were not associated with impulsivity, emotional/behavior regulations, or neurocognitive outcomes.

The findings suggest that focused skin pickers are likely to have more impairment due to their behavior compared to automatic or mixed pickers; however, overall, the groups did not differ in clinical or neurocognitive measures. Thus, it is unclear whether focused and automatic picking are particularly useful clinically in subtyping skin picking disorder.

Subtle behavioral and cognitive symptoms precede schizophrenia (SCZ) and appear in individuals with elevated risk based on polygenic risk scores (SCZ-PRS) and family history of psychosis (SCZ-FH). However, most SCZ-PRS studies focus on European ancestry youth, limiting generalizability. Furthermore, it remains unclear whether SCZ-FH reflects common-variant polygenic risk or broader SCZ liability.

Using baseline data from the Adolescent Brain Cognitive Development (ABCD) study, we investigated associations of SCZ-FH and SCZ-PRS with cognitive, behavioral, and emotional measures from NIH-Toolbox, Child Behavior Checklist (CBCL), and Kiddie Schedule for Affective Disorders and Schizophrenia (KSADS) for 9,636 children (mean age = 9.92 yrs, 47.4% female), specifically, 5,636 European, 2,093 African, and 1,477 Admixed American ancestry individuals.

SCZ-FH was associated with SCZ-PRS (b = 0.05, FDR-p = 0.02) and subthreshold psychotic symptoms (b = 0.46, FDR-p = 0.01) in European youth, higher CBCL scores (b range = 0.36–0.6, FDR-p < 0.001), and higher odds of multiple internalizing and externalizing disorders (OR = 1.10–1.22, FDR-p < 0.001) across ancestries. SCZ-PRS was associated with lower cognition across ancestries (b = −0.43, FDR-p = 0.02), higher CBCL total problems, anxious/depressed, rule-breaking and aggressive behaviors in European youth (b range = 0.16–0.33, FDR-p < 0.04), and depressive disorders in Admixed American youth (OR = 1.37, FDR-p = 0.02). Results remained consistent when SCZ-PRS and SCZ-FH were jointly modeled. Some SCZ-FH associations weakened when income-to-needs was accounted for, suggesting that SCZ-FH may capture both genetic and environmental influences.

SCZ-FH showed associations with broad psychopathology, while SCZ-PRS was associated with cognition and specific symptoms in European youth. Findings highlight their complementary role in SCZ risk assessment and the need to improve PRS utility across ancestries.