Brain and Behavior

The validation of objective neurophysiological monitoring of concussion from diagnosis to return to play has the potential to improve the clinical care of athletes. Extracted from event-related potentials (ERP), brain vital signs offer a non-invasive objective neurophysiological measure of three well established ERP responses that complement existing clinical assessments: 1) the N100 response related to auditory sensation; 2) the P300 response related to basic attention; and 3) the N400 response related to cognitive processing. The N400, in particular, has increasingly been demonstrated to be sensitive to head impact related cognitive impairment. Accordingly, brain vital sign measures were collected in n =165 rugby league players from two Australian professional National Rugby League clubs (NRL), with concussed players (n =26) being subsequently assessed over a total of five separate time points (Baseline, Day 2, Day 5, Day 10, and Day 42). This timeline aligned with acute (Day 2), NRL mandatory minimum return-to-play (RTP) guidelines (Day 10), and an extended post RTP period. Relative to baseline, the results revealed significant N400 cognitive processing latency delays at Day 2 post-concussion (p =0.002). The N400 latency delays persisted past day 5, significantly returning to baseline values at Day 10, consistent with the RTP mandatory minimum requirement. The findings indicated that neurophysiological recovery occurred in this cohort within an approximate 10-day time frame. Future studies monitoring brain vital sign changes across the trajectory of injury to recovery are needed in sports related concussion management.

Background and Objectives Transient ischemic attack (TIA) diagnosis is challenging because it relies mainly on clinical assessment and exclusion of common differential. Functional MRI (fMRI) may provide a diagnostic biomarker by detecting transient brain dysfunction not visible on conventional imaging. This pilot study aimed to characterize acute motor-task BOLD activation in patients with suspected DWI-negative TIA and compare functional patterns between confirmed TIA and alternative diagnoses. Secondary objectives were to assess longitudinal changes in activation and connectivity at 3 months. Methods In this prospective single-center study, adults presenting within 24 h of transient anterior-circulation neurological symptoms underwent conventional MRI and additional motor-task fMRI. Patients with acute DWI lesions were excluded. Final diagnosis was established after 3-month follow-up. Whole-brain analyses, individualized motor cortex region-of-interest (ROI) analyses, and generalized psychophysiological interaction (gPPI) connectivity analyses were performed during the acute phase and at 3 months. Results Eight patients were enrolled; six had complete longitudinal imaging data and were included in the final analyses. Final diagnoses were TIA (n=2), migraine aura (n=2), functional neurological disorder (n=1), and hypoglycemia (n=1). Whole-brain and ROI analyses showed reduced bilateral motor-related BOLD responses during the acute phase in both TIA patients and in the patient with hypoglycemia. In contrast, patients with migraine and functional neurological disorder exhibited less marked longitudinal changes. In TIA patients, motor cortex activation increased at 3 months, tending to normalize toward values observed in non-TIA participants. Connectivity analyses revealed heterogeneous patterns, but the 2 TIA patients demonstrated increased longitudinal connectivity between the motor cortex contralateral to symptoms and other sensorimotor regions, including supplementary motor, premotor, parietal, and postcentral cortices. Discussion These preliminary findings suggest that TIA may be associated with transient bilateral reductions in motor-network activity. Functional abnormalities appeared to improve over time, supporting the hypothesis of reversible network dysfunction. Although limited by the very small sample size, this study provides the first longitudinal assessment of emergency task-based fMRI in rigorously defined TIA and supports further investigation of acute functional MRI as a potential biomarker of transient cerebral dysfunction.

Abstract Background The neuropsychiatric sequelae (cognitive deficits, anxiety and depression) post-COVID-19 exist as part of the spectrum of the multisystemic long COVID. People with these symptoms have been shown to have worse functional outcomes. Hence, this significantly impacts the economy, primarily due to productivity losses. Yet, the precise underlying pathogenesis remains unknown, as do any diagnostic or prognostic biomarkers. Aim This study aims to identify functionally impacted brain regions in those with post-COVID-19 neurological sequelae and to evaluate how alterations in brain function relate to acute serum inflammatory mediators and brain injury biomarkers. Methods The study will utilise data from the COVID-19 Clinical Neuroscience Study (CNS), a large UK multicentre study conducted during the pandemic. This sub-study will be a secondary analysis of the COVID-19 CNS, a prospective observational study that compared COVID-19-positive participants with negative controls. Participants had an MRI, blood tested for acute serum inflammatory mediators and brain injury biomarkers, and neuropsychiatric assessment (cognitron test, PHQ-9 and GAD-7) post-acutely and at follow-up. The DPABI (Data Processing & Analysis for Brain Imaging) toolbox will be used for pre-processing and analysis of the neuroimaging data (resting state functional MRI) to obtain regional homogeneity (ReHo). The association between ReHO and neuropsychiatric symptoms, acute inflammatory mediators and brain injury biomarkers will be explored. Regression models would be used to determine the risk and protective factors for developing these symptoms. Conclusion It is anticipated that the study will provide new insights into the functional basis of post-acute COVID-19 neuropsychiatric manifestations and identify new diagnostic biomarkers. Key words: Regional Homogeneity, COVID-19, functional MRI, neuropsychiatry, biomarkers

Background: Sports betting is one of the most popular, rapidly evolving, and attractive forms of gambling. It is associated with an increased risk of gambling-related harms, including relationship difficulties, crime, and physical and mental health problems. Understanding the subjective experiences of sports betting is essential for accurately defining problematic betting and avoiding the overpathologization of the behavior. Hence, this study explored the perceptions and experiences of young men involved in sports betting in Addis Ababa, Ethiopia. Methods: We employed a qualitative study design using a phenomenological approach. In-depth interviews were conducted with thirteen purposively selected participants in Addis Ababa. Participants were adults aged 18 years or older who had engaged in sports betting within the past 12 months. They were recruited from sports betting houses. All interviews were transcribed verbatim and translated into English. The data were imported into OpenCode software and analyzed using reflexive thematic analysis, in which themes were actively generated through an iterative and interpretative process by the research team. Findings: The data resulted in five major themes: reasons for engagement in sports betting, unique and attractive features of sports betting, experiences of problematic betting, subjective harms of sports betting, and coping and recovery. Young men engaged in sports betting for financial gain, peer influence, and as a way of spending time and coping with boredom. Participants described several features that made sports betting particularly appealing, including ease of access, the ability to bet with small amounts of money, reduced interpersonal confrontation, opportunities to gamble on football, the chance to test sporting knowledge, diverse betting options, and frequent rewards and reinforcement. Experiences suggestive of problematic betting included preoccupation and extensive planning, successive betting and increased risk-taking after losses, unsuccessful attempts to quit, concealment of betting behavior, social and occupational impairment, and negative emotional experiences. Conclusion: Sports betting emerged in participants' accounts as a growing behavioral practice among young men in Addis Ababa, Ethiopia, raising concerns about gambling-related harms. While often initiated as a leisure activity, participants' narratives suggested patterns that extended beyond casual engagement and shared features commonly associated with problematic gambling. Future studies should include women and employ large-scale quantitative designs to examine the population burden and distribution of sports betting-related harms and to inform appropriate prevention and intervention strategies.

Cognitive impairment is a prevalent, disabling manifestation of Long COVID, but whether cognitive rehabilitation alters neural network organization is unknown. We examined whether a 12-week cognitive rehabilitation intervention modified resting-state connectivity within the central-executive (CEN), default-mode (DMN), and salience (SN) networks, and whether connectivity changes associated with cognitive performance. Participants were adults with prior SARS-CoV-2 infection, persistent Long COVID symptoms ([&ge;]3 months), and objectively confirmed mild-to-moderate cognitive impairment. Of 58 participants randomized, 39 (mean age 46.4; 69% women) completed neuroimaging (19 intervention, 20 control). The 12-week intervention combined virtual cognitive rehabilitation and small-group and individual sessions with computerized cognitive training. No significant group, time, or group-by-time interaction effects were observed for within- or between-network connectivity (all P > 0.22). Exploratory analyses identified nominal associations (P < 0.05) between connectivity changes and cognition; improved processing speed associated with increased CEN-DMN connectivity, greater SN-DMN connectivity associated with worse performance across processing speed, working memory, and executive function. None survived correction for multiple comparisons. Cognitive rehabilitation was not associated with detectable changes in resting-state network connectivity in long COVID-related cognitive impairment. SN-DMN connectivity may represent a marker of reduced network segregation underlying cognitive dysfunction, warranting study in larger, multimodal trials. Trial registration: NCT05498493.

Exposure to armed conflict can leave persistent effects on mental health, yet its neurophysiological correlates remain poorly characterized, particularly in populations exposed to prolonged violence outside narrowly defined post traumatic stress disorder samples. Here we examined resting state electroencephalographic activity in 122 Colombian adults, including 74 participants exposed to armed conflict and 48 controls. Eyes closed EEG was analysed for 240 seconds per participant. We quantified absolute and relative spectral power across delta, theta, alpha and beta bands and regional functional connectivity using weighted phase lag index in theta, alpha and beta. Group comparisons were adjusted for age, education, sex and assessment year, with correction across 78 EEG contrasts. Median occipital and global alpha power was lower in exposed participants, although adjusted estimates were close to the null and confidence intervals were broad. Temporal theta relative power was lower in exposed participants at nominal significance, but this association did not survive Holm correction. No spectral power or regional connectivity contrast remained significant after multiple testing correction. Exploratory associations between EEG measures and MoCA performance were modest in participants with confirmed scores. These findings provide a systematic characterization of resting EEG after exposure to armed conflict in a population shaped by prolonged violence and displacement. They also indicate that large or widespread alterations in resting spectral power and connectivity were not detectable with the current sample and analytical framework, while defining candidate signals and methodological priorities for larger studies of conflict related brain health.

Hypoxia impairs cognitive function, yet its effects on navigation and intrinsic brain activity remain poorly understood. This study investigated whether a continuous exposure to hypoxia (CH) or an intermittent exposure to hypoxia (IH) differentially influence navigation performance and resting-state electroencephalography (EEG) in healthy young adults. Seventy-two participants completed sham (FiO2 = .209) and hypoxia (FiO2 = .13) sessions during either a one hour of CH or IH intervention. Navigation was assessed using the Spatial Performance Assessment for Cognitive Evaluation (SPACE), while resting-state EEG was recorded before and after the intervention in a subset of participants (n = 40). EEG spectra were parameterised into periodic (alpha and beta power and central frequency) and aperiodic (exponent and offset) components. Aligned rank transform (ART) analyses of variance examined effects of hypoxia and intervention group, while linear regression determined whether reductions in peripheral oxygen saturation (SpO2) predicted changes in navigation or EEG. Hypoxia impaired multiple components of navigation, increasing path integration distance error and egocentric pointing angle error irrespective of intervention group, while mapping accuracy was preferentially impaired following IH and perspective taking performance following CH. Hypoxia also reduced alpha and beta power, beta central frequency, and aperiodic exponent, while aperiodic offset and alpha central frequency remained stable. The reduction in aperiodic exponent was primarily evident following IH, suggesting that the temporal pattern of oxygen delivery may influence specific neurophysiological responses. Contrary to our hypothesis, SpO2 reduction did not predict individual differences in navigation performance or EEG activity. These findings demonstrate that brief, moderate hypoxic exposure can disrupt allocentric and egocentric components of spatial navigation while selectively altering periodic and aperiodic features of intrinsic brain activity.

Inhibitory control is an essential executive function that encompasses both the stopping of an action in response to an unexpected stop signal (reactive response inhibition) and slowing of responses in anticipation of stopping (proactive response inhibition). Fronto-basal-ganglia circuits are thought to differentially contribute to response inhibition, with the indirect pathway implicated in proactive inhibition. Given the high expression of dopamine D2 receptors in the indirect pathway, pharmacological blockade of D2 receptors is expected to impact proactive inhibition, as indicated by response times on Go trials. The current study aimed to investigate this experimentally and study the effect of 600 mg of sulpiride, a D2 receptor antagonist, on behavioural and electrophysiological measures of proactive and reactive inhibition in humans. Human participants (N=24) completed an anticipated response version of the stop-signal task on either sulpiride or placebo in a double-blind within-subjects design. Sulpiride led to increased variability of Go response times and attenuation of the frontocentral negativity/readiness potential, considered to be a signature of proactive inhibition. In contrast, sulpiride had no effect on stop-signal reaction time or event-related potential components associated with reactive inhibition. These findings suggest that D2 receptor blockade selectively alters processes involved in proactive inhibition while leaving reactive inhibition unaffected, consistent with a key role for the indirect basal ganglia pathway in proactive response inhibition.

Background: Determining the cause of death in electrocution is often challenging at autopsy, particularly when characteristic external electrical marks are absent. Reliable internal markers are scarce, and the neuropathological changes associated with electrocution remain underexplored. Objective: To identify and characterize histopathological alterations in the brain in cases of fatal electrocution and evaluate their diagnostic utility. Methods: A prospective observational study was conducted on 12 autopsy cases, including 7 confirmed electrocution deaths and 5 non-electrocution deaths (control). Brain tissue samples from multiple regions were processed using H&E and Golgi Cox staining. Histopathological parameters, including neuronal morphology, vascular changes, haemorrhage, and dendritic architecture, were evaluated. Results: Electrocution cases demonstrated neuronal destruction, axonal ballooning, focal hemorrhages, and dendritic disruption. Cerebellar involvement with Purkinje cell damage. Conclusion: Comprehensive neurohistological technique may helpful in evaluation neuronal damage in electrocution death. Neuropathological findings, particularly neuronal and dendritic injury, may serve as supportive evidence in determining cause of death when external signs are absent. Keywords: Electrocution, Neuropathology, Golgi Cox stain, Forensic histopathology, death.

Disorders of consciousness (DoC) are characterised by marked reductions in cerebral glucose metabolism, but the specific cellular and neurochemical processes driving this impairment remain unclear. To elucidate these mechanisms, a multimodal imaging approach combining [18F]-fluorodeoxyglucose positron emission tomography (FDG-PET) and magnetic resonance spectroscopy (MRS) was applied to the posterior medial cortex (PMC) in 15 DoC patients and 14 healthy controls. Regional FDG metabolic index (FDG-MI) values and MRS concentration estimates of glutamate plus glutamine (Glx), {gamma}-aminobutyric acid (GABA+), total N-acetylaspartate (tNAA), total creatine (tCr), and total choline (tCho) were compared between groups and evaluated against Coma Recovery Scale-Revised (CRS-R) scores at baseline and follow-up (mean 127 days). Patients demonstrated reductions within the PMC in Glx, tCr, and tNAA concentrations, as well as a reduced Glx/GABA+ ratio. Local FDG-MI was substantially reduced in patients and correlated positively with tNAA and tCr. Furthermore, baseline tCho concentrations positively predicted long-term clinical recovery, as indexed by changes in CRS-R scores at follow-up. These findings suggest that macroscopic glucose hypometabolism in DoC may be linked to disrupted intracellular mitochondrial energy production pathways and a shift towards relative synaptic inhibition in the PMC. Moreover, the association between choline levels and behavioural recovery may point to the relevance of retained structural synthesis capacity for functional outcomes.

Trauma-related intrusive memories (TRIMs) are a core symptom of posttraumatic stress disorder and cause significant distress and impairment for trauma-exposed individuals due to their vivid sensory features that intrude on ongoing thought. These phenomenological properties point to a neuropathology that spans autobiographical memory, spontaneous thought, and sensory perception. The hierarchical organization of the cortex maximally segregates the default mode network (DMN), which supports autobiographical memory and ongoing thought, from the sensory cortices (SC). Accruing evidence implicates altered interactions between the DMN and SC in PTSD and TRIMs, suggesting a breakdown in this segregation. We sought to test whether diminished DMN-SC segregation, indexed by a shorter functional distance between the DMN and SC within cortical connectivity gradients, was associated with the vividness and intrusiveness of TRIMs. One-hundred eight trauma-exposed adults completed two weeks of ecological momentary assessments (EMAs) of TRIM properties followed by resting-state fMRI. Gradient analysis of cortical functional connectivity was performed to compute the Euclidean distance between resting-state networks. Pearson correlations revealed an association between a shorter DMN-SC distance and greater TRIM vividness and intrusiveness, with multivariate models indicating a specificity for intrusiveness. Importantly, the DMN-SC distance was not associated with clinician-rated symptom severity and explained unique variance above and beyond conventional functional connectivity measures. These findings suggest that a loss of functional segregation between the DMN and SC - a core organizational feature of the cortical hierarchy - is associated with the intrusive sensory vividness of TRIMs, offering insights into candidate mechanisms of and neurotherapeutic targets for intrusive trauma memories.

Objective: Mindfulness is a robust predictor of mental health, yet the psychometric properties of the short-form Five Facet Mindfulness Questionnaire (FFMQ-15) have not been examined in Iranian populations. This study evaluated the psychometric properties, factor structure, and diagnostic utility of the FFMQ-15 among medical sciences students. Participants: A total of 348 students (178 females, 170 males) from Kermanshah University of Medical Sciences participated. Methods: Participants completed the FFMQ-15, Penn State Worry Questionnaire (PSWQ), Difficulties in Emotion Regulation Scale (DERS), and Emotion Regulation Questionnaire (ERQ). Data were analyzed using exploratory and confirmatory factor analyses, composite reliability, and ROC curve analysis. Results: Both EFA and CFA supported the five-factor model, revealing a culturally unique item loading pattern. The FFMQ-15 demonstrated strong convergent and discriminant validity. ROC analysis indicated acceptable diagnostic accuracy for distinguishing high- and low-worry groups (AUC = 0.72, 95% CI: 0.66-0.78). Conclusions: The FFMQ-15 demonstrated acceptable psychometric properties in Iranian medical students. The non-reactivity facet exhibited cultural variability, suggesting that cross-cultural adaptation is essential. The instrument shows promise for screening in high-stress educational settings.

Background/Aims: Pre-stroke depression has been shown to be associated with worse functional outcomes and depression after stroke. However, it is not currently well understood whether pre-stroke mood disorders (e.g., depression, anxiety, mood and psychotic disorders, substance use disorder) are associated with withdrawal of life-sustaining treatment (WOLST) after a severe stroke. Methods: This was a retrospective cohort study within the Tufts Vascular Neurology Registry of patients hospitalized with severe acute ischemic stroke (AIS, defined as NIHSS [&ge;]10) or severe nontraumatic intracerebral hemorrhage (ICH, defined as ICH score [&ge;]2) between 2018 and 2022. Multivariate logistic regression was performed to identify predictors of WOLST. Results: This study included 405 patients with severe stroke. Patients who opted for WOLST were more likely to be older, female, have AIS, and experience more severe strokes. In an adjusted analysis (basic demographics, stroke type), a pre-stroke mood disorder was associated with WOLST (OR 2.15, 95% CI 1.11-4.15). In models stratified by stroke type (AIS vs. ICH) and adjusted for stroke severity, WOLST was associated with age in both groups and with mood disorder in patients with ICH. The WOLST event rate was higher in the ICH group (19% vs 11%). Conclusion: Pre-stroke mood disorder was associated with increased rates of withdrawal of care after severe stroke in this patient population. Opportunities to actively treat depression may be useful to include in goals of care discussions to mitigate the potential impact of this factor in decision-making. Consistent with prior studies, we observed a higher proportion of WOLST in older, female, and ICH patients. Future studies regarding the quality and content of goals of care discussions may help elucidate the differing effects of pre-stroke mood disorders on WOLST by stroke type seen in this study.

Background: Excessive inflammation in early phases post-ischemic stroke is associated with poor long-term outcome and increased stroke recurrence. Interventions capable of downregulating persistent states of inflammation could improve recovery and prevent secondary stroke. Cardiovascular exercise (CE) has well-established anti-inflammatory effects but its capacity to attenuate the exaggerated inflammatory response triggered by ischemic stroke is unclear. Methods: We investigated the impact of eight weeks of CE on the serum concentration of inflammatory mediators in the early subacute phase post-stroke. Seventy-one patients with firstever ischemic stroke were randomly assigned to moderate-to-vigorous CE (n=45) or standard care (SC) (n=26). Concentrations of CRP, IL-6, IL-8, IL-10, TNF- and IL-1{beta} were measured at baseline and after the interventions. Differences between groups were analyzed with linear mixed models adjusted for age and sex. Results: Compared with the CE group, the SC group showed significant increases in IL-6 ({beta}=0.585, 95% CI=0.164-1.006, p=0.0073), IL-8 ({beta}=0.160, 95% CI=0.004-0.317, p=0.0447), and TNF- ({beta}=0.0845, 95% CI=0.0137-0.1553, p=0.0206). The SC group also showed greater increases in CRP ({beta}=0.250, 95% CI=-0.407, 0.906, p=0.4499) and IL-10 ({beta}=0.251, 95% CI=-0.024, 0.527, p=0.0729) but group differences were not significant. IL-1{beta} levels remained stable and differences between groups were not significant ({beta}=-0.008, 95% CI=-0.058, 0.042, p=0.7618). Conclusions: When introduced in the early subacute phase of stroke recovery, moderate-tovigorous CE mitigates increases in inflammation, but the effect differs across mediators. To what extent reducing the inflammatory response in the early stages post-stroke with CE can impact longterm recovery and stroke recurrence needs to be determined.

The hippocampus is particularly vulnerable to hypoxia, yet freedivers, who repeatedly undergo voluntary breath-hold hypoxia, do not appear to show the memory impairments commonly reported after involuntary hypoxic exposure. We investigated whether freediving training is associated with functional connectivity reorganization at the whole-brain and hippocampal levels, and whether hippocampal connectivity relates to preserved episodic memory performance. Seventeen male recreational freedivers underwent fMRI before and after a 7-month standardized training period, and 20 matched aerobic-trained controls were assessed at baseline. Functional connectivity analyses examined (i) whole-brain ROI-to-ROI connectivity, (ii) seed-to-voxel connectivity from the bilateral hippocampus and selected cortical seeds, and (iii) associations between hippocampal connectivity and episodic memory. Compared with controls, freedivers showed distinct connectivity patterns during apnea and rest. After training, whole-brain analyses revealed reorganization involving salience, frontoparietal, sensorimotor, visual, and cerebellar systems. Hippocampal analyses showed reduced connectivity with sensorimotor and default mode regions, alongside increased connectivity with cerebellar and visual areas, with stronger effects after training. In freedivers, specific post-training hippocampal connectivity was associated with episodic memory performance. These findings suggest that repeated voluntary hypoxia during freediving training is associated with selective functional reorganization of hippocampal and large-scale brain networks. This pattern may reflect adaptive neuroplasticity linked to preserved episodic memory under intermittent hypoxic exposure.

Introduction: Neuroinflammation is a known pathophysiologic mechanism in multiple sclerosis and a proposed mechanism in fibromyalgia and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Positron Emission Tomography (PET) imaging of the translocator protein (TSPO) has been widely used to measure neuroinflammation, though second-generation ligands are highly sensitive to a single nucleotide polymorphism, rs6971, resulting in high, mixed, and low affinity binders. It is unknown whether this polymorphism is associated with neuroinflammatory disorders. Materials and Methods: Eighty-six total participant genotypes for TSPO binding affinity were identified through Sanger sequencing (30 fibromyalgia, 21 ME/CFS, 11 multiple sclerosis, and 24 healthy controls). Associations between patient group and genotype were assessed with Fishers Exact test. Associations between genotype and symptom severity from self-report questionnaires were assessed with Kruskal-Wallis tests. Results: In the present study individuals with fibromyalgia, (ME/CFS), or multiple sclerosis were more likely to have a mixed- or low-affinity genotypes compared to healthy controls. Presence of the low or mixed genotypes were also associated with greater self-reported fatigue severity and depressive symptoms. Discussion: These findings should be confirmed in larger samples but suggest functional consequences of rs6971 polymorphism that may be related to the pathophysiology of pain and fatigue illnesses.

Background: Stroke survivors frequently experience post-stroke depression (PSD) and post-stroke anxiety (PSA), which may be underexamined by clinicians if patient mood status between discharge and follow-up is unknown. Digital monitoring may enable early identification of mood disturbances. Ecological momentary assessments (EMA) have been tested to capture mood fluctuations in patients regular environments, but no standardized procedure for monitoring PSA or PSD has been developed. Objective: Determine the feasibility and validity of EMA for evaluating subacute PSA and PSD in non-severe stroke patients. Methods: Patients with non-severe stroke discharged home responded to daily smartphone EMA questions concerning mood and activity for twelve weeks until follow-up. Questions based on symptoms of anxiety and depression were used to derive EMA Anx and EMA Dep indices, computed over five 15-day intervals. Convergent validity was assessed using follow-up Generalized Anxiety Disorder-7 (GAD-7) and Centre for Epidemiological Studies-Depression (CES-D) scores. Logistic regression models predicted PSA and PSD status at follow-up, with baseline models comprising stroke severity, age, sex, and mood status, to which EMA Anx or Dep were added. Results: Data from 118 patients were analyzed. EMA adherence was moderate, with 89 patients (75.4%) responding on 75 or more days. Correlations between EMA Anx and GAD-7 and between EMA Dep and CES-D generally strengthened at later intervals, with the average mood index generally showing the strongest associations. Adding EMA data from the third time interval (31-45 days) significantly improved model fit beyond the baseline models (Anxiety: {chi}-square = 7.08, p = 0.008, {delta}R-square = 0.060; Depression: {chi}-square = 28.0, p < 0.001, {delta}R-square = 0.256). Discussion: EMA is feasible in mild-to-moderate stroke patients and may facilitate early identification of post-stroke mood disturbances. Further analyses in more diverse populations are required to validate these findings.

Background In Kenya, stroke is one of the top five causes of mortality, with a high rate of inpatient mortality. The American Heart Association (AHA) and American Stroke Association (ASA) translated scientific evidence into evidence-based clinical practice guidelines aimed at reducing inpatient mortality and improving the quality of care for stroke patients. Despite the proven benefits of the ASA stroke guidelines in improving stroke care, translation of the guidelines in various settings remains a key challenge. This study aimed to quantify the gap between evidence-based recommendations and current stroke care practices in a peri-urban referral facility in Kiambu, Kenya. The study was conducted at xxxxxxxxxx Hospital, a peri-urban referral facility in Kiambu County, Kenya. Methods: We reviewed records of stroke patients attending xxxxxxxxxxx from January 1, 2020, to December 31, 2023. The study evaluated acute stroke management practices and secondary prevention against the 2019 American Heart Association/American Stroke Association (AHA/ASA) Guidelines for the Early Management of Acute Ischemic Stroke. Results: The median distance travelled by stroke patients to the facility was 47.8 kilometres; further, the median onset-to-presentation time was 24 hours. The study evaluated eight clinical practices against the ASA guidelines. The facility lacked a dedicated stroke unit. Remarkably, patients arriving within the therapeutic window for intravenous alteplase and thrombectomy did not receive these treatments. Secondary prevention measures, including discharge on an antiplatelet regimen, were moderately adhered to; among the 86 eligible ischemic stroke patients, 67 (77.9%) were correctly discharged on aspirin. Similarly, 84/123 (68.3%) of the patients were discharged on statin therapy. Conclusion: Evidence-based stroke care recommendations were minimally adhered to at this peri-urban referral facility in Kiambu, Kenya. Contribution: This study quantifies the gap between evidence-based stroke care recommendations and current clinical practice in a peri-urban referral facility in Kenya, providing context-specific evidence to inform quality improvement initiatives and guideline implementation efforts in similar resource-constrained settings.

BACKGROUND: One in three adolescents with a concussion history report experiencing long-lasting somatic, sleep, emotional, and/or cognitive disturbances (persisting symptoms after concussion (PSaC)). Cognitive difficulties, such as attentional problems, are common symptoms and can interfere with ongoing development. Clinically, psychiatric symptoms also present in youth with PSaC. A concussion causes diffuse functional and microstructural alterations to neural networks. To develop targeted treatments for PSaC (e.g., neurostimulation), we need to understand how and where structural alterations and neural dysfunction intersect to cause long-lasting symptoms. OBJECTIVES: 1) Identify functional and microstructural properties in intrinsic connectivity networks, as well as neuropsychological outcomes, that differentiate adolescents with concussion with PSaC from those who do not have PSaC. 2) Determine whether neural activity within intrinsic connectivity networks mediates the relationship between network microstructure and specific neuropsychological features in adolescents with concussion. METHODS: CAMBY is a prospective study of adolescents aged 12 to 18 years with a history of concussion. Participants are allocated based on recovery status (PSaC vs. No-PSaC (recovered controls)). Advanced structural (magnetic resonance imaging; MRI) and functional (magnetoencephalography; MEG) neuroimaging and neuropsychological measures will be collected one month or more after concussion. Microstructural and functional features will be computed within intrinsic connectivity networks, then compared between PSaC and recovered control groups and related to symptom domains and neuropsychological profiles. IMPACT: This will be the first study to integrate MRI, MEG, and neuropsychology in adolescents with PSaC to identify disrupted networks underlying PSaC. This observational study is a necessary step towards future clinical trials that accurately target promising therapeutic neurostimulation protocols.

Background: Stroke imposes substantial mortality and socioeconomic burden in India, particularly among younger adults. However, prospective evidence on the prognostic value of baseline clinical and radiomics features for mortality prediction remains limited. Objective: To assess mortality at 28, 90, 180, and 365 days after stroke; characterize survival patterns across stroke subtypes and vascular territories; and identify baseline demographic, clinical, and radiomics predictors of mortality. Methods: This prospective cohort study recruited consecutive patients with stroke admitted to a tertiary care hospital in Mangalore, India. Demographic, clinical, laboratory, and radiomics features were collected at admission, and mortality was assessed at 28, 90, 180, and 365 days. Kaplan Meier analysis was used to compare survival across stroke subtypes and vascular territories, while Cox proportional hazards regression was used to identify independent baseline predictors of mortality. Results: Among 63 confirmed stroke cases, 38 (60%) had ischemic stroke (IS) and 25 (40%) had haemorrhagic stroke (HS). Within the middle cerebral artery (MCA) territory, HS patients demonstrated better survival than IS patients due to a greater burden of adverse baseline characteristics such as previous stroke, atrial fibrillation, and higher lesion volume in the IS-MCA subgroup. The combined clinical-radiomics model demonstrated superior prognostic performance than individual models, with higher concordance indices and consistently lower Akaike Information Criterion values. In the combined model, stroke severity (aHR = 2.35, 3.0, 2.93, 2.41) and DWI texture heterogeneity of lesion (aHR = 2.35, 2.11, 2.24, 2.10) were the strongest predictors of mortality across all time points. The CT attenuation heterogeneity (aHR = 1.81, 28 days; 1.76, 90 days; 1.80, 180 days) of lesion and age (aHR = 1.48, 365 days) were also significant predictors. Conclusion: The radiomics features provide critical complementary information to clinical parameters for predicting 28-day mortality, unlike during mid- to long-term follow-up where their incremental contribution appears to be limited. Our results may have important implications in resource-constrained settings for supporting personalized post-stroke management and rehabilitation.