Suicide is the second leading cause of death among youth, with growing evidence linking higher ambient temperatures to increased suicidality - a concerning trend as global temperatures rise. Sleep disruption is a theorized mechanism, though clinical evidence is lacking.

We performed a cross-sectional analysis of 5,590 pediatric patients (3-18 years) presenting to a psychiatric emergency department with and without suicidality (December 2018-March 2023). Seven-day averages of mean and minimum daily ambient temperatures and precipitation were obtained at home addresses from the PRISM Climate Group dataset. Logistic regression assessed insomnia as a moderator and mediator of the temperature-suicidality relationship, controlling for sociodemographic, diagnostic, and environmental variables. Negative controls included modeling suicidality using hypersomnia-temperature and insomnia-precipitation interactions.

Mean and minimum daily temperatures moderated the temperature-suicidality relationship only in those with insomnia (Mean Temperature: RR: 1.06 per 5°C [95% CI 1.01-1.06], p = 0.015; Minimum Temperature: RR: 1.06 per 5°C [95% CI 1.01-1.06], p = 0.010). Minimum temperature, a proxy for nighttime temperature, was associated with suicidality through insomnia in a mediation model (Indirect Pathway: OR: 1.05 [95% CI 1.00-1.11], p = 0.045), though mean temperature was not. No significant moderation occurred modeling suicidality with hypersomnia-temperature or insomnia-precipitation interactions.

This is the first clinical evidence that insomnia influences the heat-suicidality relationship in youth. Limitations include cross-sectional data that cannot establish temporal directionality of associations, heterogeneous suicidality outcomes, self-reported sleep data, and pandemic-era data collection. Larger mechanistic analyses of temperature, sleep, and suicidality are needed to understand climatic mental health impacts and develop interventions.

Acupuncture has shown clinical benefits in post-stroke rehabilitation, yet its central neural mechanisms remain incompletely understood. In particular, how cortical activation, inter-regional functional connectivity, and brain network topology are modulated during electroacupuncture stimulation has not been systematically characterised. This study aimed to investigate the central effects of verum electroacupuncture (VE) applied to the non-dominant hand in healthy adults. In a randomized, crossover design, functional near-infrared spectroscopy (fNIRS) data were collected from 24 participants during VE and sham electroacupuncture (SE) sessions. Cortical activation was assessed using a general linear model (GLM), functional connectivity (FC) was analysed using lagged cross-correlation, and brain network topology was examined using graph-theoretical metrics. No significant differences in cortical activation were observed between VE and SE. During the needles retention phase, VE significantly reduced functional connectivity between R-MPFC and right primary somatosensory cortex (R-PSC), and between middle MPFC and R-PSC. Graph-theoretical analysis revealed decreased clustering coefficient and increased small-worldness under VE. These findings suggest that VE may optimise brain networks through an connectivity-topology mechanism. Brain networks shifted from excessive localisation toward higher integration. This study establishes a baseline central response profile in healthy individuals and provides theoretical support for the application of electroacupuncture in post-stroke upper-limb rehabilitation. Trial registration: ITMCTR, TRN: ITMCTR2025000595, Registration date: 19 March 2025.

Epilepsy and sleep disorders are highly prevalent conditions that frequently coexist, exerting reciprocal adverse effects through shared neurobiological mechanisms.

We conducted a narrative review of the literature addressing the bidirectional relationship between epilepsy and sleep disorders, aiming to provide a comprehensive synthesis of its neurophysiological basis, clinical implications, and therapeutic consequences.

The epilepsy-sleep relationship is mediated by multiple neurobiological mechanisms, including thalamocortical network dynamics, circadian clock gene regulation, adenosinergic and orexinergic tone, synaptic homeostasis, and glymphatic clearance. A key pathophysiological concept underlying this relationship is that NREM sleep promotes interictal epileptiform discharges and seizure propagation through thalamocortical synchronization, whereas REM sleep exerts a protective effect. Epileptic activity disrupts both sleep macro- and microarchitecture, reducing total sleep time, sleep efficiency, and REM sleep, increasing wake after sleep onset, and destabilizing NREM microarchitecture as reflected by altered cyclic alternating pattern rates. Conversely, sleep disturbances lower the seizure threshold and contribute to disease progression: sleep deprivation is an independent seizure-precipitating factor, and comorbid obstructive sleep apnea further lowers the seizure threshold through intermittent hypoxia and arousal instability. Specific epileptic syndromes with a privileged sleep relationship are also reviewed, including sleep-related hypermotor epilepsy, epileptic encephalopathy with spike-wave activation in sleep, and self-limited childhood focal epilepsies. The differential diagnosis between NREM parasomnias and sleep-related epilepsies remains challenging; the diagnostic workup should always include a thorough clinical history characterizing the episodes, followed by video-polysomnography, which represents the gold standard. From a therapeutic standpoint, antiseizure medications exert heterogeneous effects on sleep architecture, and polytherapy is independently associated with worse sleep quality; targeting sleep disturbances therefore represents a modifiable strategy capable of improving seizure control, cognitive function, and quality of life.

A multidisciplinary approach integrating systematic screening for sleep disorders, optimization of antiseizure medication timing and selection, treatment of comorbid obstructive sleep apnea, and behavioral sleep interventions has the potential to meaningfully improve outcomes in patients with epilepsy. Wider implementation of these strategies in routine clinical practice is both a priority and an opportunity.

Mental health among medical trainees has typically been framed as an individual deficit, addressed through resilience training and counseling services. This perspective examines how the hidden curriculum within Chinese psychiatry training may shape psychological safety and professional identity formation. Drawing on psychological safety theory, hidden curriculum scholarship, Bronfenbrenner's ecological systems theory, and recent empirical literature on medical trainee distress in China, we propose a theoretically derived and empirically testable conceptual model through which experiences of vulnerability may become socially and professionally invisible. The proposed vulnerability-to-invisibility process describes four interconnected phases: the encounter with vulnerability, perceived or enacted prohibition of emotional expression, internalization of silence, and potential fragmentation of professional identity. Existing evidence supports several constituent components of this pathway, but direct empirical evidence establishing the complete sequence remains limited. We therefore call for institutional reforms that embed psychological safety into clinical training, including protected reflective spaces, reflective faculty modeling, peer support, and curriculum-integrated mentorship, while emphasizing adaptive emotional regulation rather than forced suppression.

Reproductive life stages, menopausal symptoms, and hormonal exposures are increasingly recognized as potential determinants of cognitive outcomes in women. However, these associations remain largely understudied in Latin American and Caribbean (LAC) populations. In this systematic review, we identified 18 observational studies published between 2003 and 2025. Of these, 16 were conducted across 13 LAC countries and two were conducted among latina women in the United States. Evidence was organized across four reproductive life stages domains: reproductive history, menopausal hormone therapy use, type of menopause and menopausal symptoms, and postmenopausal factors. Most LAC studies were cross-sectional and demonstrated substantial methodological heterogeneity. Across studies, shorter reproductive span, earlier menopause, higher parity, surgical menopause, and greater menopausal symptom burden were generally associated with poorer cognitive performance or higher odds of mild cognitive impairment. Some studies suggested favorable associations between menopausal hormone therapy use and cognitive outcomes. Postmenopausal factors, such as sarcopenia and obesity, as well as a longer duration of menopause, were predominantly linked to poorer cognitive outcomes. Only one population-based cohort evaluated incident dementia, underscoring the scarcity of longitudinal evidence in the region. Overall, the evidence suggests that reproductive life stages in LAC women are meaningfully associated with cognitive outcomes, reflecting the influence of hormonal transitions, menopausal characteristics, and postmenopausal health within distinctive regional contexts. However, the predominance of cross-sectional designs and limited regional representativity, coupled with a lack of integrated physiological indicators, reveal a substantial knowledge gap. Longitudinal and regionally representative cohorts incorporating standardized assessments of reproductive life stages alongside comprehensive cognitive measures are essential to understanding how reproductive life stages shape cognitive outcomes in LAC women. Systematic review registration: The systematic review was registered in the Open Science Framework (OSF). Registration DOI/unique identifier: https://doi.org/10.17605/OSF.IO/ME7XK.

Concussion disrupts brain connectivity, and effective treatments remain limited. Mindfulness-based interventions (MBIs) may influence functional connectivity (FC) of networks affected by concussion, but pediatric trials are lacking. This study investigated whether an app-delivered MBI produced greater FC changes than a sham condition across the default mode (DMN), salience (SN), and central executive (CEN) networks.

This randomized clinical trial (NCT05105802) recruited participants aged 12.00-17.99 years from the emergency department or interdisciplinary concussion clinic, then randomly assigned them to MBI or cognitive sham. Brain imaging sessions occurred at 72 h and 4 weeks post-concussion. Region-of-interest and seed-to-voxel analyses examined Group × Time interactions in FC across DMN, SN, and CEN (p < 0.050 _FDR ).

Thirty-six participants were included (MBI: n = 16, median [IQR] age = 14.23 [13.52-15.65] years, 31% female; Sham: n = 20, median [IQR] age = 14.05 [13.13-16.26] years, 45% female). Intention-to-treat analyses revealed significant Group × Time interactions across networks. DMN-CEN FC patterns differed, with MBI participants showing diminished FC. Within DMN, four clusters showed significant interactions (p < 0.050 _FDR ), three exhibiting larger FC reductions at 4 weeks in MBI participants. MBI participants showed greater FC increase in one SN cluster (p = 0.040 _FDR ) and larger FC decrease in one CEN cluster (p = 0.024 _FDR ) at 4 weeks. Per-protocol analyses identified one significant DMN cluster (p < 0.001 _FDR ) where MBI participants exhibited greater FC increases.

Mindfulness-based intervention training led to changes in FC in networks implicated in concussion recovery. Larger studies are needed to support these findings.

https://clinicaltrials.gov/study/NCT05105802, identifier NCT05105802.

Muslim mental health is an emerging field of inquiry in the global South. Understanding how mental health conditions are interpreted within diverse Muslim communities is important for culturally responsive psychological care.

This qualitative study explored psychologists' experiences of providing services to Muslim clients in the Western Cape, South Africa, and explored psychologists' accounts of explanatory models of mental health conditions encountered in therapeutic practice. Semi-structured interviews were conducted with 15 clinical and counseling psychologists practicing in the Western Cape. Data were analyzed using Reflexive Thematic Analysis.

Three themes were constructed. First, psychologists emphasized the importance of understanding Muslim clients within their broader sociocultural and historical context, particularly the enduring influence of Apartheid, migration histories, intergenerational trauma, and institutional mistrust. Second, psychologists reported encountering diverse explanatory models among Muslim clients, including interpretations of distress in relation to religiosity, supernatural influences, stigma, personal weakness, and biomedical understandings. These explanatory models were described as shaping emotions such as fear, guilt, and shame, as well as pathways to help-seeking and engagement with treatment. Third, psychologists highlighted the importance of culturally responsive practice, including reflexive engagement with clients' religious worldviews, ongoing self-education, culturally informed supervision, and ethical collaboration with Muslim religious leaders.

The findings suggest that explanatory models are not solely individual beliefs about MHC but are embedded within broader religious, familial, historical, and sociopolitical contexts. By exploring psychologists' accounts of therapeutic encounters with Muslim clients in the Western Cape, this study extends explanatory-model scholarship by highlighting how collective histories and relationships with systems of care shape understandings of mental health and help-seeking.

Type 2 diabetes mellitus (T2DM) is frequently accompanied by complex brain microstructural abnormalities and cognitive decline. Conventional diffusion tensor imaging (DTI) metrics can reflect both tissue diffusion properties and extracellular free-water effects, complicating the interpretation of T2DM-related brain changes. We aimed to characterize free-water-corrected diffusion alterations in white matter (WM) and cortical gray matter (GM) and examine their associations with cognitive performance and fasting blood glucose.

We enrolled 48 patients with T2DM and 48 healthy controls (HCs). Diffusion measures included conventional fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD), together with free-water-corrected FA (FAt), free-water-corrected MD (MDt), free-water-corrected AD (ADt), and free-water-corrected RD (RDt), as well as the free-water fraction (FW), estimated using a free-water elimination (FWE) DTI model. Tract-based spatial statistics (TBSS) was used to evaluate all nine diffusion metrics in WM, whereas gray matter-based spatial statistics (GBSS) was used to evaluate six metrics in the cortical GM skeleton (AD, MD, RD, ADt, MDt, and RDt). Voxel-wise association analyses were performed using FMRIB Software Library (FSL) randomise based on a general linear model with nonparametric permutation testing to examine the relationships of imaging metrics with fasting blood glucose and Mini-Mental State Examination (MMSE) scores, while adjusting for age, sex, and total intracranial volume in the primary models; sensitivity models additionally included diagnostic group as a covariate.

Compared with HCs, patients with T2DM showed widespread diffusion abnormalities across the WM and GM skeletons, including lower FAt and higher MDt, ADt, and RDt. No skeleton-wide between-group difference in the estimated FW was detected. In the primary analyses, higher fasting blood glucose was associated with higher FW in selected WM regions and greater cortical GM diffusivity, whereas lower MMSE scores were associated with widespread WM and GM diffusion abnormalities.

T2DM-related diffusion abnormalities persisted after free-water correction, whereas no skeleton-wide between-group difference in the estimated FW was detected. Integrating FWE with complementary spatial analyses of WM and cortical GM may help characterize diffusion-derived brain phenotypes and their clinical correlates in T2DM.

Adult ADHD and autism assessment services increasingly receive clinically heterogeneous referrals in which the sequelae of childhood adversity may overlap with neurodevelopmental presentations. The distribution and clinical significance of adverse childhood experiences (ACEs) in this referral population remain insufficiently characterized.

This retrospective cross-sectional cohort study analyzed routinely collected clinical data from 389 adults who attended either the ADHD or the autism diagnostic pathway of a regional National Health Service (NHS) Adult ADHD and Autism Service. The analytic sample consisted of 233 adults with a definitive diagnostic outcome at data extraction; 149 were awaiting an outcome, six had an inconclusive outcome, and one underage case was excluded. ACE exposure was measured with the 10-item ACE Questionnaire. Psychiatric symptom burden was assessed with routinely administered screening instruments (PHQ-9, GAD-7, AUDIT, DAST-10, MDQ, HELPS and IPDS). The primary analysis examined the association between ACE score, analyzed as a continuous variable, and diagnostic outcome, with adjustment for age, gender and assessment pathway in binary logistic regression; all other analyses were exploratory.

Forty-seven participants (20.2%) received a diagnosis of ADHD or autism and 186 (79.8%) did not meet DSM-5 criteria. The mean ACE score was 3.10 (SD = 2.59), and 39.7% of participants reported four or more ACEs, compared with 8.3% in an English national household survey. Participants who were not diagnosed reported higher ACE scores than participants who were diagnosed (3.37 vs. 2.04; Hedges g = 0.52, 95% CI 0.19-0.84, p = 0.002). In the adjusted model, each additional ACE was associated with lower odds of receiving a neurodevelopmental diagnosis (odds ratio 0.85, 95% CI 0.73-0.99, p = 0.040). The proportion diagnosed declined across ACE categories from 35.6% (no adversity) to 6.2% (six or more ACEs). ACE scores correlated positively with depressive symptoms (r = 0.37), anxiety symptoms (r = 0.28) and drug use scores (r = 0.27), but not alcohol use, and were higher among participants screening positive for possible personality disorder, head injury and mood disorder. In an exploratory model additionally adjusting for depressive symptoms and personality disorder screening status, the ACE association attenuated and was no longer statistically significant, indicating that it is not independent of concurrent psychiatric symptom burden.

ACE exposure in this referral cohort was substantially higher than English population estimates and was associated with diagnostic non-confirmation and with greater psychiatric symptom burden. These findings support consideration of childhood adversity within trauma-informed formulation during adult neurodevelopmental assessment. Prospective studies incorporating direct measures of trauma-related psychopathology are needed to determine whether trauma-related mechanisms contribute to neurodevelopmental-like presentations. The cross-sectional retrospective design precludes causal inference.

Effective management of drug-resistant tuberculosis requires molecular assays that not only detect Mycobacterium tuberculosis but also identify resistance-associated variants, support drug-level interpretation, and indicate when broader confirmatory testing is needed. This narrative review applies a mutation-to-drug-to-decision framework to distinguish assay validity, exact-variant detection, drug-level inference, and decision impact. We synthesize evidence on target accessibility, minority-allele preservation, multiplexing, direct-specimen testing, and sequencing enrichment, emphasizing how these factors shape clinical interpretability. Current evidence remains dominated by analytical studies, isolate-based evaluations, and small direct-specimen investigations, with prospective multicenter treatment-impact validation still lacking. Population-level benchmarks indicate incomplete biological coverage for compact target regions, reaching approximately 92.6% for rpoB RRDR-based rifampicin detection, 85.4% for katG codon 315 plus the inhA promoter for isoniazid, and 84.7%-88.2% for gyrA/gyrB-based fluoroquinolone detection. Allele-specific CRISPR is therefore best suited to rapid rule-in of selected resistance-associated variants, while dispersed or heterogeneous mechanisms require broader molecular or phenotypic assessment. CRISPR should complement WHO-recommended rapid molecular testing and targeted next-generation sequencing rather than replace established molecular or phenotypic methods.