Introduction:
Stroke remains a major global cause of death and long-term disability, emphasizing the need for rapid and accurate diagnosis to support timely clinical decisions.

Methods:
This study proposes a hybrid deep ensemble framework that integrates convolutional neural networks (ResNet50) and transformer-based models (Swin Transformer) to detect stroke from multimodal neuroimaging data. A publicly available Kaggle dataset comprising 5,336 CT and MRI scans from 230 participants (113 females, 117 males) was used, including 2,695 stroke and 2,641 control images. Features extracted from both networks were fused into a unified representation and reduced using PCA-based cumulative weighted neighborhood component analysis (CW-NCA). The reduced features were classified using a stacking ensemble of k-nearest neighbors, a support vector machine (SVM), XGBoost, and multilayer perceptron (MLP), with a linear SVM as the meta-learner.

Results:
The proposed model achieved a validation accuracy of 94.10%. For the Normal class, the precision, recall, and F1-score were 93.80%, 94.33%, and 94.06%, respectively. For the Stroke class, the precision, recall, and F1-score were 94.40%, 93.88%, and 94.14%, respectively. The model demonstrated balanced performance across both classes, indicating robustness and reduced bias.

Discussion and Conclusion:
Compared with single-model CNN or transformer methods, the hybrid ensemble exhibited superior generalization and class stability. These findings suggest that the proposed framework can serve as a promising decision-support system for early stroke detection, helping clinicians achieve faster and more reliable diagnoses.

This trial aimed to evaluate the effectiveness of the sport-based exercise therapy program (sET) combined with usual care (UC) compared to UC alone in adults with an acquired brain injury (ABI). In a single-blind randomized controlled trial, 23 adults with an ABI, precisely with stroke and traumatic brain injury (mean age 59.6±10.3 years), were assigned to sET+UC (n=11) or UC (n=12). The intervention included sixteen 60-minute racket sport sessions plus UC, matched in duration and frequency with the control group. Outcomes included health-related quality of life (SF-36), upper limb motor control (FM-UE), functional capacity (6MWT, 10MWT), mobility (TUG), balance (BBS), and physical activity participation (GPAQ). Significant between-group differences were observed following the intervention. Participants in the sET+UC group demonstrated substantial improvements in both physical (p=.027, r=.46) and mental (p=.001, r=.71) components of the SF-36, and in FM-UE scores (p=.004, r=.60), all with moderate to large effect sizes. In addition, the intervention group showed statistically significant gains (p<.05, r>.5) across functional capacity, balance, and overall physical activity participation. In contrast, the UC group showed only minimal, non-significant changes across all domains. This trial provides evidence supporting the integration of sport-based exercise therapy into conventional rehabilitation for adults with ABIs. The program not only enhanced physical and functional outcomes but also improved quality of life and physical activity engagement. These findings underscore the value of combining sport-based exercise as a complementary strategy to UC for enhancing multiple domains in this population. Furthermore, these findings emphasize the potential to optimize patient care by facilitating the transition from supervised exercise in rehabilitation community-grounded sports, filling a critical gap post-rehabilitation, thereby addressing critical gaps post-rehabilitation such as risks of sedentary behavior and social isolation. Larger studies with long-term follow-up are needed to confirm the sustainability and wider applicability of this approach.

Introduction:
Colloid cysts of the third ventricle are uncommon but clinically significant. Some remain silent and are found incidentally, while others cause sudden neurological deterioration. In a few cases, this can be fatal without urgent treatment. Surgery is the mainstay, although complications are well recognized. We reviewed our experience over 15 years.

Methods:
We carried out a retrospective review of patients treated surgically for colloid cysts between 2010 and 2025. Hospital records were used to collect information on demographics, clinical features, operative details, and complications. Descriptive statistics were applied. This was a small cohort.

Results:
Fifteen patients were included. The mean age was 30 years (9 males, 6 females). More than half were diagnosed in the emergency department (53%). Four patients (27%) were detected incidentally and three (20%) were diagnosed in clinic. Headache was the most common symptom (87%). Nausea and vomiting were noted in 47%. Seizures occurred in two patients, and three presented with coma or rapid decline. Papilledema was documented in four. All underwent surgical resection, and some required perioperative shunts. Early complications were frequent, affecting 53%. Late complications were even more frequent, recorded in 87%. Memory problems were reported in 60% of patients. The median hospital stay was 11 days.

Conclusions:
In our setting, colloid cysts showed varied presentations. Surgery was effective, but complications—especially cognitive issues—were common. Careful perioperative planning and follow-up remain essential.

Modifications of cell adhesion and remodeling of the extracellular matrix (ECM) occur in the brain under physiological conditions (e.g., during embryonic development and in neuronal plasticity) and in pathological microenvironments (e.g., in hypoxia-dependent angiogenesis in cancer or strokes, or with the migration of the tumor cells themselves). Glioblastoma is the most common and devastating type of primary brain tumor, for which the standard of care has largely remained unaltered since 2005. Here, we wanted to study possible changes in both ITGA1 (which encodes the integrin alpha-1 protein, a receptor for collagen) and NID2 (which encodes the nidogen-2 protein in basement membranes, a protein that binds to collagen) mRNA levels based on anatomic features classified as pseudopalisading cells around necrosis (PAN), microvascular proliferation near the pseudopalisading cells (MVP), and cellular tumors (CTs) in human glioblastoma. Primary data were collected from the Ivy Glioblastoma Atlas Project, a public anatomic transcriptional database, from in situ hybridization (ISH) in glioblastoma blocks. To better compare the results, we selected images with similar architectures to PAN, MVP, and CT regions. Our results indicate that ITGA1 and NID2 genes are poorly expressed in the PAN region, which contrasts with their very high expression in the adjacent MVP zone. In addition, the ITGA1 and NID2 genes are expressed at low-medium levels in the CT areas underlying the MVP region. Other genes with the same biological function, such as BCAN and DDR1, do not show significant area-dependent transcriptional variations. Therefore, our results suggest that cell–matrix adhesion could be decreased in the PAN structure (stimulating pseudopalisading cell migration) but increased in the MVP region (promoting ECM deposition and stabilizing the vascular bed growth). Furthermore, all these results also suggest that elevated ITGA1 and NID2 expression is positively correlated with increased neovascularization, and that they could be a potential target for therapeutic intervention.

Disturbances in oxygen concentration, particularly hypoxia, occur in different pathological conditions, as in tumors, and hypoxia can also cause brain damage in strokes. One tissue response to low oxygen levels is the activation of angiogenesis. In glioblastoma, the most common primary brain tumor in adults, with a poor prognosis, microvascular proliferation in response to hypoxia is common. The Public Ivy Glioblastoma Atlas Project – Allen Institute for Brain Science contains an expression data set for 37 genes enriched in glioblastoma, and we have verified that at least 5 (ADGRL4, BTG1, ENPEP, ESM1, and STC1) are directly involved in angiogenesis. This study aims to investigate mRNA levels of these genes in different histologically-defined glioblastoma regions. To better compare the results obtained from in situ hybridization (ISH) in glioblastoma blocks, we selected images with a similar tissue architecture, specifically perinecrotic pseudopalisading regions with an underlying zone of a cellular tumor. Our primary results show that ADGRL4, ENPEP, ESM1, and STC1 genes were mainly expressed (in medium-high levels) in the endothelium of hyperplastic blood vessels that accumulated near the pseudopalisading cells. Nevertheless, the BTG1 gene (the protein that positively regulates endothelial cell differentiation and angiogenesis) was ubiquitously expressed (also at medium-high levels), both in the previous vessel regions and in the pseudopalisading around necrosis areas and the rest of the tumor. We used DDR1 as a control gene that is not expressed in endothelial cells. Our preliminary data also suggest a similar spatial distribution of ADGRL4, BTG1, ENPEP, ESM1, and STC1 expression in patients with different molecular subtypes of glioblastoma: classical, proneural, classical-mesenchymal, and neural-proneural. We conclude that ADGRL4, ENPEP, ESM1, and STC1 genes appear to be preferentially expressed in the endothelium of the glioblastoma microvasculature; however, BTG1 appears to show a ubiquitous distribution within the tumor. The functional significance and possible therapeutic relevance remain to be demonstrated.

Glioblastoma is the most common primary brain tumor in adults. With a poor prognosis, its treatment has barely advanced in the last twenty years. High cell densities limit the availability of nutrients/oxygen, leading to necrosis and/or endothelial and microvascular proliferation. However, it exhibits a high capacity for survival, in which glioblastoma stem cells and autophagy may be involved. The objective of this study was to evaluate, among the different histological structures of glioblastoma, the expression of BNIP3 (its product induces autophagy (mitophagy) by direct interaction with LC3B-II) and one of its transcriptional regulators, HIF1A (the O₂-regulated protein promotes adaptation to hypoxia). The results were obtained from the analysis of in situ hybridization (ISH) images in glioblastoma sections, stored in the free database Ivy Glioblastoma Atlas Project. All patients we studied showed high levels of BNIP3 mRNA in the perinecrotic pseudopalisading areas, and medium expression in the vessel walls and even in the infiltrating tumor region. From the pseudopalisading regions around necrosis, BNIP3 transcription decreased significantly as we advanced into the tumor. Interestingly, only some patients showed expression (and in these cases, high expression) of HIF1A in the pseudopalisading formations, although HIF1A was expressed, at variable levels, in the vessel walls. These results indicate anatomy-dependent levels for the mRNA encoding BNIP3 and HIF1A in glioblastoma. Furthermore, they suggest strong mitophagy activation in the pseudopalisading cells, as well as mechanisms regulating BNIP3 mRNA levels independent of HIF1A expression. These mechanisms could be other transcriptional factors, such as E2Fs, FOXO3, TP53, and NFKB, and/or a regulation by stabilization of the HIF1A protein under hypoxia. Our data could also be applied to other brain pathologies, where low oxygen levels contribute to tissue damage.

Background: Sleep disruption is a prevalent yet under-recognised issue among stroke patients, with growing evidence suggesting its adverse impact on neurological recovery and rehabilitation. This study explores the causes of in-hospital sleep disturbances and evaluates post-discharge care-seeking behaviours in a stroke patient cohort.

Methods: A retrospective cohort study was conducted at Wrexham Maelor Hospital, North Wales, using data from the Sentinel Stroke National Audit Programme (SSNAP), the Welsh Clinical Portal, and the EPOC from March 2024 to March 2025. A structured questionnaire was administered post-discharge to assess self-reported sleep quality across three time periods: pre-stroke, during hospitalisation, and after discharge. Contributing factors to sleep disturbance and patient interactions with healthcare providers regarding sleep concerns were also examined.

Results: Among 225 stroke patients, environmental factors were the most frequently reported causes of in-hospital sleep disruption, with noise (n=139) being the leading factor, followed by clinical interventions (n=82), lighting (n=36), anxiety/stress (n=23), pain (n=22), and disability (n=19). Despite widespread disturbances, only 13.3% of patients reported discussing sleep issues with their general practitioner post-discharge, and fewer than 10% received any formal management for sleep-related concerns.

Conclusion: The findings highlight a clear gap between the clinical importance of sleep and its recognition in stroke care. Environmental disruptions during hospitalisation are a key modifiable contributor to poor sleep, yet patient concerns are seldom addressed in post-discharge settings. Integrating routine sleep assessments and environmental interventions into stroke care pathways is essential for promoting recovery and improving quality of life.

Approximately 20% of concussion/mild traumatic brain injury (mTBI) patients experience persistent post-concussion symptoms (PPCSs) beyond four weeks. Functional neurological disorder (FND) and somatic symptom burden are frequent, overlapping contributors in such cases, yet practical guidance for differentiating and managing these mechanisms remains limited.

We present a clinical framework integrating literature review, neurobiological models (central sensitization, fear-avoidance, predictive processing), and observations from a specialized neuropsychiatry practice. Case prototypes illustrate functional versus somatic presentations. Clinical experience from recent consecutive evaluations (October 2024–October 2025) informed symptom patterns and treatment approaches, including tailored medication, specialized rehabilitation, and cognitive reframing.

Among patients evaluated for PPCS during this period, the majority showed prominent somatic symptom burden, with a substantial minority meeting FND criteria. Functional presentations were associated with greater somatic burden and psychiatric comorbidities. Anecdotally, most of those who engaged in cognitive reframing and individualized care strategies reported improvement at follow-up (as measured by CGI-I), although formal outcome data are needed. These patterns, combined with existing literature supporting the preventive role of early education after concussion, suggest a potential opportunity for targeted early intervention.

Somatic and functional features are prevalent contributors to PPCS. A structured, neurobiologically informed approach can clarify symptom mechanisms and guide care. Differentiating these symptom drivers early and communicating a positive, reversible narrative may improve outcomes. Formal retrospective and prospective studies are warranted. Based on these insights, we are developing a randomized controlled trial to assess whether brief early cognitive framing can reduce PPCS incidence and healthcare utilization. Furthermore, while functional-specific rehabilitation protocols exist, there is a need for validated somatic-focused interventions.

Introduction: Some metabolites of aromatic amino acids are known to be of microbial origin [https://doi.org/10.1038/nature24661]. Elevated concentrations of microbial 4-hydroxyphenyllactic acid (p-HPhLA) in cerebrospinal fluid (CSF) have previously been detected in post-neurosurgical patients with signs of secondary bacterial meningitis in comparison to those without signs of secondary bacterial meningitis [https://doi.org/10.3390/jpm12030399].

Objectives: To assess the ratio of p-HPhLA in serum and CSF samples collected simultaneously from patients with long-term sequelae of severe brain damage with suspected secondary bacterial meningitis.

Methods: Blood (n=29) and CSF (n=29) samples were collected simultaneously within one day from patients (n=15) with long-term sequelae of severe brain damage with suspected secondary bacterial meningitis. Group I included 16 paired serum and CSF samples from patients without secondary bacterial meningitis (n=11, 8 men, 3 women, aged from 21 to 82); group II included 13 paired serum and CSF samples from patients with secondary bacterial meningitis (n=4, 2 men, 2 women, aged from 22 to 65). p-HPhLA concentrations were detected using HPLC-MS/MS.

Results: Median p-HPhLA concentrations in serum: group I—975 nmol/l; group II—1676 nmol/l; Mann-Whitney U-test, p-value, - 0.008. Median p-HPhLA concentrations in CSF: group I—414 nmol/l; group II—2578 nmol/l; Mann-Whitney U-test, p-value, < 0.001. In group I, p-HPhLA concentrations in serum were higher than those in CSF in 13 of 16 samples; in group II, p-HPhLA concentrations in serum were lower than those in CSF in all samples.

Conclusion: The obtained results may confirm the hypothesis of the microbial origin of p-HPhLA in CSF in patients with secondary bacterial meningitis.

Sweetener consumption has increased considerably in recent decades, driven by the growing demand from consumers seeking low-calorie products for weight control and especially from diabetic patients who require safe sweetener alternatives without affecting their glucose levels. However, the latest scientific evidence seems to indicate that the continued consumption of various sweeteners could significantly alter the gut microbiota, triggering consequences that go beyond metabolic health and could affect sleep quality.

Among the most used non-caloric sweeteners in the food industry are sucralose and saccharin. Several studies have shown that prolonged consumption of these sweeteners can significantly alter the composition of the gut microbiota. In particular, a decrease in beneficial bacteria such as Lactobacillus and Bifidobacterium has been observed, accompanied by an increase in potentially pathogenic microorganisms such as Clostridium difficile and Escherichia coli. This dysbiosis generates a chronic low-grade inflammatory environment and contributes to the deterioration of glucose metabolism, factors that negatively impact the regulation of the gut–brain axis. Consequently, these alterations could interfere with the neuroendocrine mechanisms involved in sleep, promoting the development of disorders such as insomnia, sleep fragmentation, and decreased subjective sleep quality.

The aim of this systematic review is to synthesize the current scientific evidence on the impact of artificial sweeteners on the gut microbiota and their potential involvement in sleep disorders. The underlying biological mechanisms will be analyzed and the clinical relevance of these interactions will be discussed, laying the groundwork for future research that will contribute to the development of dietary recommendations and therapeutic strategies aimed at modulating the microbiota to improve sleep health.