Glioblastoma is the most common malignant primary brain tumor in adults. Gliomas infiltrate and destroy surrounding brain tissue, leading to neurological deficits such as speech and visual disturbances, hemiparesis, cranial nerve palsies, personality changes, and impaired consciousness. These symptoms may mimic acute stroke; however, 20-40% of patients initially diagnosed with stroke in the emergency department (ED) are later found not to have experienced an acute cerebrovascular event. Brain tumors account for approximately 5% of such stroke mimics. The aim of the study was to present a clinical case of brain tumor mimicking stroke. We present a 71-year-old woman admitted with suspected stroke due to impaired verbal communication, confusion, disorientation, and transient mild rightsided weakness. Symptoms had progressed over one week. Brain computed tomography revealed a hypodense lesion in the medial left temporal lobe, and magnetic resonance imaging suggested a high-grade glioma infiltrating deep structures. Intravenous dexamethasone was initiated. Navigated biopsy confirmed glioblastoma on histopathological examination. The patient was not eligible for oncological treatment and underwent supportive care, including rehabilitation. At discharge, she was ambulatory with caregiver assistance and remained on long-term dexamethasone with proton pump inhibitor (PPI) prophylaxis. Despite advances in therapy, glioblastoma carries a poor prognosis, with approximately 10% five-year survival.
Aim: To analyse contemporary global approaches to training nursing personnel for the public health sector, focusing on the integration of competency-based, interprofessional, and practice-oriented models, and to evaluate their strategic relevance to the transformation of national health systems. Materials and Methods: A systematic literature review and narrative synthesis were conducted using international scientific databases (PubMed/Medline, Scopus, Web of Science) covering 2010-2026, with an analytical focus on publications from 2021-2026. The search strategy was guided by Boolean logic and targeted MeSH terms. Of the 120 records initially identified, 35 core sources, including global strategic guidelines from the WHO and ICN, met the strict inclusion and exclusion criteria and were selected for final qualitative analysis. Conclusions: Transitioning from traditional clinical education to integrated instructional models (CBE, IPE, and the ADDIE framework) is crucial for developing a resilient workforce. For transforming national systems, such as Ukraine’s, managing this transition through adaptive, asynchronous e-learning under emergency conditions ensures the attainment of critical population-based competencies, with a focus on epidemiological surveillance and community-based preventive care.
Post-traumatic stress disorder (PTSD) is a multifactorial neuropsychiatric condition characterized by persistent disturbances in fear processing, emotional regulation, and memory. Increasing evidence indicates that dysregulation of glutamatergic neurotransmission plays a crucial role in both the development and persistence of PTSD. Glutamate, the primary excitatory neurotransmitter in the central nervous system (CNS), is essential for synaptic plasticity and the formation of traumarelated memories. The aim of this study was to provide an integrated and critical synthesis of current knowledge on glutamatergic dysfunction in PTSD, with particular emphasis on its neurobiological, clinical, and therapeutic implications. This article is a narrative review of the literature published between 2017 and 2025 was conducted. Databases such as PubMed, Scopus, and Web of Science were searched for experimental, clinical, and neuroimaging studies investigating glutamatergic signaling in PTSD. The reviewed studies indicate that chronic stress disrupts glutamate homeostasis, leading to increased extracellular glutamate concentrations and impaired synaptic clearance. These alterations result in excessive activation of ionotropic receptors, particularly N-methyl-D-aspartate (NMDA) receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, promoting calcium influx and neuronal dysfunction. Such processes affect key brain regions, including the amygdala, hippocampus, and prefrontal cortex, contributing to impaired fear extinction and heightened emotional reactivity. Importantly, glutamatergic dysregulation does not occur in isolation but interacts dynamically with neuroinflammatory pathways, altered inhibitory transmission, and dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis. In conclusion, altered glutamatergic neurotransmission represents a central mechanism in PTSD pathophysiology. Its role in synaptic plasticity, neuronal vulnerability, and network dysregulation highlights its potential relevance as a diagnostic and therapeutic target. Future research should focus on integrating glutamate-related biomarkers with mechanism-based therapeutic interventions in order to improve diagnostic precision and treatment outcomes in PTSD
Aim: To systematically analyse empirical data on the mental health of Ukrainian children in the context of armed conflict; to conduct a comparative analysis with research on the consequences of the Second World War; to examine long-term social consequences; and to analyse the state of the psychosocial support system, with particular attention to the trauma-informed approach as its methodological foundation. Materials and Methods: Narrative review with elements of comparative analysis. Databases searched: PubMed/MEDLINE, Scopus, Web of Science, PsycINFO. Included: empirical studies and systematic reviews/meta-analyses (2022-2026) on children and adolescents (0-18 years) in war or post-conflict settings with measurable mental health, behavioural, or developmental outcomes; comparative studies on children from the Second World War era, with no time restrictions. Supplemented by institutional reports and national Ukrainian research. Conclusions: Ukraine is facing a psychiatric and social crisis of historic proportions for European children. An effective response requires long-term systemic investment in psychosocial support grounded in the trauma-informed approach, with priority for underserved groups (the youngest children, orphans, children of the mobilised), deinstitutionalisation, anti-stigma education, and urgent funding for longitudinal research.
Post-traumatic stress disorder (PTSD) is associated with persistent dysregulation of cellular stress pathways and altered neuronal signaling within limbic and prefrontal circuits. Increasing evidence indicates that activation of endoplasmic reticulum stress responses, oxidative imbalance, and inflammasome signaling contribute to sustained neurobiological alterations underlying PTSD symptomatology. Stress-induced activation of inositol-requiring enzyme 1 (IRE1) and activating transcription factor 6 (ATF6) interacts with inflammatory mediators such as interleukin-18 (IL-18) and interleukin-1β (IL-1β), amplifying neuroimmune responses. Activation of the NOD-like receptor family pyrin domain containing 3 inflammasome (NLRP3 inflammasome) and caspase-1 promotes cytokine maturation and microglial activation, leading to impaired synaptic plasticity. These mechanisms are accompanied by alterations in glutamatergic and gammaaminobutyric acid (GABA) signaling, oxidative stress imbalance, and dysregulation of the hypothalamic–pituitary–adrenal axis. Neuroimaging data demonstrate volumetric and microstructural changes in the hippocampus, amygdala, and prefrontal cortex in chronic PTSD, suggesting structural correlates of prolonged inflammatory and stress-related activity. Biomarker studies further indicate associations between inflammatory mediators, coping strategies, sleep disturbances, and illness duration. These findings support the concept that increased cellular stress responses and altered neuronal signaling are central components of PTSD pathophysiology rather than secondary epiphenomena. Understanding the interaction between endoplasmic reticulum stress, inflammasome activation, oxidative imbalance, and neurotransmitter dysregulation may improve biomarker-based diagnostics and facilitate development of targeted therapeutic interventions.
