Introduction:

Seizure-related loss of consciousness (LOC) in pediatric epilepsy significantly impacts safety, cognitive development, and quality of life. The thalamus is believed to play a central role in sustaining consciousness via its integrative cortical connectivity. Disruption of thalamocortical networks may underlie impaired awareness during seizures, yet mechanistic insights remain limited. Stereo-electroencephalography (sEEG) offers high-resolution intracranial recordings that enable in vivo exploration of these neural dynamics. Here, we present a protocol designed to systematically evaluate thalamocortical functional connectivity during seizures with and without LOC in pediatric patients with drug-resistant epilepsy. This protocol serves as a foundation for future hypothesis-driven investigations and network-targeted therapeutic strategies.

Methods:

Postoperative CT scans are co-registered with preoperative MRI to localize and label electrode contacts. sEEG data are exported from the Natus system into Brainstorm for preprocessing and quantitative analysis. Recordings include at least 10 minutes of pre-ictal, ictal, and post-ictal data. Seizures with and without LOC are identified and time-marked using synchronized video-EEG. LOC severity is scored independently by two experienced reviewers. Functional connectivity is assessed via Coherence (Coh) and maps are generated to visualize thalamocortical network dynamics.

Results:

Fourteen pediatric patients underwent thalamic sEEG implantation. Etiologies included focal cortical dysplasia, periventricular nodular heterotopia, neonatal HIE, and non-lesional epilepsy. Pre-implant hypotheses included temporal, frontal, insular, and multifocal seizure onset. Thalamic sampling included anterior and pulvinar nuclei. Interictal thalamic abnormalities were present in most of the patients. A protocol of the analysis was created and will be presented as a flow chart with the major analysis steps in the poster.

Conclusions:

This protocol-based approach enables rigorous investigation of thalamocortical connectivity and its role in LOC during epileptic seizures. Ongoing analyses will evaluate frequency-specific functional connectivity associated with altered awareness. Findings from this study may enhance patient-specific neuromodulation strategies and advance our understanding of consciousness disruption in epilepsy.

Background: Few studies have explored whether sevoflurane impacts cerebral vascular reactivity (CVR) or increases postoperative cognitive dysfunction in ischemic moyamoya disease (IMMD). We aimed to evaluate the effects of sevoflurane anesthesia on cerebral blood flow (CBF) and CVR in IMMD.

Methods: This prospective cohort study recruited 15 patients with IMMD and 17 with intraspinal space-occupying lesions, as healthy controls (HCs), between September 2023 and March 2024 in Peking University International Hospital. CBF in the whole brain and anterior (ACA), middle (MCA), and posterior (PCA) cerebral arteries was measured using 3.0 T magnetic resonance imaging (MRI) with pulsed arterial spin labeling (PASL) sequences. Measurements were taken in the awake and sevoflurane-anesthetized states (sedation depth BIS 40-60). CVR was then calculated. PASL data were processed using SPM8 and ASLtbx. Continuous variables were compared using t-tests; categorical variables were compared using chi-squared tests.

Results: Under sevoflurane anesthesia, CBF and CVR decreased in IMMD (P<0.05) in the whole brain and bilateral ACA, MCA, and PCA regions. Whole-brain CBF was higher in IMMD than in the HCs pre-anesthesia and decreased post-anesthesia (P < 0.05); there was little change pre- and post-anesthesia in the HCs (P > 0.05). CVR differed pre- and post-anesthesia in the IMMD group (P<0.05) in all arteries except the left MCA. No significant difference in CVR was observed in the HCs pre- and post-anesthesia.

Conclusions: PASL-MRI is a feasible, non-invasive, quantitative tool for assessing global and regional CBF changes in mechanically ventilated patients under anesthesia. Sevoflurane anesthesia may further reduce CVR in IMMD, potentially increasing cerebral ischemia risk during and after surgery. Inhalational anesthetics should be carefully selected for these patients. Alternative drugs, or techniques that optimize CBF regulation, should be considered to improve postoperative recovery and long-term outcomes.

Probiotics are live microorganisms that, when administered in adequate amounts, confer a health benefit on the host. Their use has become increasingly common as they help maintain a balanced gut microbiota and support immune function. In recent years, attention has also turned to the communication pathways between the gut and the brain, which suggest that probiotics might influence not only digestion and immunity but also inflammation, pain, and recovery after neurological injury.

The aim of this review was to explore how probiotic supplementation affects quality of life in patients after brain surgery and whether it plays a role in reducing lower back pain. We searched for scientific studies in the international databases PubMed, ScienceDirect, MEDLINE (EBSCOhost), CINAHL Ultimate, and Wiley Online Library. The search and selection process was shown using a PRISMA flow diagram, and the quality of the studies was assessed according to an eight-level hierarchy of evidence. A thematic synthesis was then carried out.

Altogether, eleven studies met the inclusion criteria—five dealing with lower back pain and six focusing on patients after brain surgery. The results show that probiotics may have some positive effects, such as reducing inflammation and infection risk, shortening hospital stay, and helping bowel function recover faster. However, the evidence for improving overall quality of life or reducing back pain is still limited and inconsistent.

In conclusion, probiotics show potential as supportive agents in improving recovery and general health, but more well-designed clinical studies with larger samples, defined strains, and standardized evaluation methods are needed to better understand their role in pain management and postoperative recovery.

Introduction:

Traumatic brain injury (TBI) and HIV-associated neurocognitive impairment (NCI) are the leading causes of long-term disability, with effects on cognitive, motor, and psychological functioning. Even with improved acute care and antiretroviral therapy, successful and individualized neurorehabilitation is a continuing need. New technologies, specifically artificial intelligence (AI), virtual reality (VR), and telerehabilitation platforms, present new potential to enhance outcomes through individualized interventions and decision-making in real-time.

Methodology:

This review synthesizes evidence from recent clinical trials, AI model performance analysis, and neurorehabilitation trials for TBI as well as HIV-related NCI. The AI algorithms developed for TBI were compared on the basis of diagnostic accuracy, prognostic models, and rehabilitation optimization. The computational neurorehabilitation paradigms were evaluated for their capacity to merge the digital flow of data among patients, clinicians, and predictive systems. Cognitive rehabilitation devices, such as immersive games and distant training systems, were assessed regarding accessibility, customization, and compliance in HIV-impacted populations.

Results:

AI models exhibited up to 95.6% accuracy in mortality and functional outcome prediction in TBI. AI-enhanced neuroimaging enhanced diagnostic sensitivity. Non-invasive brain stimulation, VR, robot-assisted therapy, and computer-based training were partially effective in TBI rehabilitation. Technology-enabled cognitive rehabilitation enhanced adherence and motivation in HIV-related NCI, especially with gamified and immersive settings. Yet disparities in digital access and the absence of large-scale trials were observed.

Conclusion:

AI and computational neurorehabilitation have important potential to propel individualized therapy in TBI and HIV-related NCI. Satisfying ethical issues, interoperability of data, and availability will be crucial for their broader clinical deployment. Future research should emphasize solid, large-scale trials to prove and extend these technology-based interventions.

Background:

Synaptic plasticity in neurodegenerative disorders (NDs), cognitive impairment, and mental health conditions is regulated by brain-derived neurotrophic factor (BDNF). Even healthy individuals have different levels, which are affected by complex epigenetic, inflammatory, and metabolic regulation. BDNF expression changes are associated with both typical and abnormal aging, as well as mental health conditions. These changes affect brain areas that are crucial for memory, such as the hippocampus and the parahippocampal cortex. Neurotrophins (NTs), including nerve growth factor (NGF) and BDNF, are essential for neuronal differentiation via tropomyosin receptor kinase (Trk) and the p75 neurotrophin receptor (p75NTR). Dysregulated NT signaling contributes to synaptic dysfunction and neuroinflammation.

Objective:

This systematic review synthesizes preclinical evidence of the potential of naturally derived compounds to modulate NTs for neuroprotection and their incorporation into novel foods.

Methodology:

A review of major databases found studies that examined the impact of dietary polyphenols and other bioactive substances on NT signaling, oxidative stress, inflammation, and neuronal plasticity.

Results:

Compounds such as epigallocatechin gallate, resveratrol, curcumin, quercetin, and flavanols can positively impact NTs, reducing reactive oxygen species (ROS)/reactive nitrogen species (RNS), enhancing cell survival, and increasing the expression of trophic factors such as Nrf2, NGF, and vascular endothelial growth factor (VEGF) in neural stem cells. However, their bioavailability, optimal dosage, and dietary interactions require further research.

Conclusions:

The consumption of BDNF-promoting foods can potentially stimulate BDNF synthesis, support optimal neurotransmission, and fortify neural plasticity. Evidence supports a polyphenol-rich diet for preventing NDs and promoting brain health. Observational studies consistently support the protective effects of polyphenols on brain health through their impact on the gut–brain axis.

Introduction: Regular physical activity modulates neuroplasticity and protects against age-related cognitive decline. However, the acute effects of exercise on higher-order language functions remain poorly defined. This study investigated how a single moderate-intensity cycling session influences lexical-semantic processing speed in middle-aged adults.
Methods: Forty-one healthy participants (mean age 43.6 ± 1.7 years; 22 women, 19 men) were randomly assigned to an exercise group (n = 20; 15 min cycling at 65% HRmax) or control group (n = 21; passive video viewing). Cognitive performance was assessed before and after intervention using a lexical decision task involving real and pseudowords (1 s presentation). Reaction times (RTs) and accuracy were recorded. Heart rate (HR) was continuously monitored to verify exertion level. Participants were additionally divided into younger (<40 years) and older (>40 years) subgroups to assess age-related differences in cognitive response.
Results: Heart rate analysis confirmed adequate workload and recovery (p ≤ 0.001). Acute exercise significantly reduced RT for both pseudowords (d = 0.60; p ≤ 0.0001) and real words (d = 0.39; p ≤ 0.0001), whereas the control condition produced smaller but reliable improvements (pseudowords d = 0.40; p ≤ 0.001; words d = 0.27; p ≤ 0.01). Age-stratified analysis indicated more pronounced improvements in participants > 40 years (p ≤ 0.05). These behavioral changes suggest transient enhancement of cortical efficiency in semantic decision-making, possibly mediated by increased cerebral perfusion and neurotrophic signaling.
Conclusion: A brief session of moderate-intensity aerobic exercise enhances semantic processing speed, reflecting rapid neuroplastic modulation of cortical language networks. The effect was evident across both sexes and most pronounced in adults over 40, suggesting that short aerobic activity may serve as a simple, non-pharmacological intervention to preserve semantic memory and cognitive fluency during midlife and aging.

Athletes often face acute, chronic, or extreme stress that activates the sympathetic nervous system–hypothalamic–pituitary–adrenal axis and elevates cortisol and catecholamines. Short bursts may aid arousal, but prolonged activation undermines dorsolateral prefrontal cortex (DLPFC)-mediated attention, working memory, and executive control. Precisely how each stress type affects cognition and its neural basis remains unclear.

Objective

To synthesise evidence (2000-2025) on how different stress states affect athletes’ cognitive performance and to outline the associated neural mechanisms.

Methods

Following PRISMA, we searched CNKI, PubMed, Web of Science, SPORTDiscus, and PsycINFO (Feb 2000-Feb 2025). Keywords combined “stress”, “athletes”, “cognitive/executive function”, and “neural mechanism”. From 1,253 hits, 46 studies met inclusion criteria (athlete sample; stress manipulation; and cognitive or neural outcomes) and were qualitatively synthesised.

Results

1) Acute stress impairs attentional allocation and decision speed in combative/team sports, increasing critical-moment errors; 2) fine-skill athletes (e.g., gymnastics and shooting) show reduced motor precision under acute stress; 3) chronic stress in endurance athletes slows processing and reaction times and heightens cognitive fatigue; 4) working memory and attentional control prove most vulnerable, with marked capacity loss in high-pressure settings; 5) high acute stress disrupts sustained attention, causing lapses; 6) prolonged chronic stress erodes executive functions—planning and flexibility—and raises impulsivity; 7) stress lowers response inhibition, increasing interference errors; 8) imaging: acute stress down-regulates DLPFC and up-regulates amygdala/anterior cingulate cortex activity; 9) neurochemistry: elevated cortisol, norepinephrine, and dopamine weaken prefrontal control; 10) electroencephalography: diminished P300 amplitudes indicate reduced attentional resources; 11) psychological interventions (mindfulness and cognitive restructuring) ease anxiety and bolster attention/flexibility; 12) physiological techniques (breathing drills and progressive muscle relaxation) reduce heart rate and cortisol, improving adaptation; and 13) transcranial direct current stimulation shows promise for restoring attentional control and decision-making under stress.

Conclusion
Stress-related neuroendocrine shifts weaken prefrontal control, eroding athletes’ attention, working memory, and executive skills. Future studies should track long-term and individual effects and develop targeted, multi-modal countermeasures.