Objectives. To develop a morphological classification of neuronal damage for use in practical activities by researchers, pathologists, and forensic experts.

Material and methods. The neurons of the cerebral cortex of 30 experimental animals (Wistar rats) were studied. Of these: with circulatory arrest N=10, with clozapine poisoning in combination with alcohol N=20 (clozapine dose 150 mg/kg, alcohol dose 5 ml/kg); morphological material of the human cerebral cortex was studied in subarachnoid hemorrhages (SAH) N=23, sudden cardiac death N=10, coronavirus infection N=18. Histological preparations were stained with hematoxylin and eosin, according to Nissl, according to Feulgen (for DNA), according to Brachet (for RNA and RNP), caspase-3 was detected by immunohistochemistry.

Results. A morphological classification of neuronal damage was proposed, including: decentralization of the nucleus within a neuron, morphological changes in the nucleolus, dark neurons, chromatin remodeling, lipofuscinosis, neuronal edema, Nissl substance lysis, neuronal calcification, neuronophagia, necrosis, and neuronal apoptosis. Functional disorders that occur in the studied variants of neuronal alteration were considered. As a result of developing neuronal damage, the function of the neuronal cytoskeleton, synthesis of ribosome subunits, synthesis of ribonucleoproteins, and DNA reparation are impaired, apoptosis is activated, lysosomes are damaged, the formation of reactive oxygen species is activated, and irreversible forms of neuronal damage (neuronophagia, necrosis, apoptosis) are recorded.

Conclusion. The proposed morphological classification complements existing classifications based on the study of molecular markers of neuronal damage and can be used in experimental studies and in the practical work of pathologists and forensic experts.

The aim of the study was to identify potential predictors of functional outcome (FO) in patients with subtypes of ischemic stroke (IS) who did not receive reperfusion therapy.

Materials and methods. A prospective study included 229 patients with ischemic stroke divided . into three groups based on the IS subtype: Group 1 — 84 patients with cardioembolic IS; Group 2 — 65 patients with atherothrombotic IS; Group 3 — 80 patients with lacunar IS. Changes in the modified Rankin Scale (mRS) scores were considered as FO criteria calculated as the difference between the scores on admission and on the 21^st day after IS onset — ∆mRS. In order to optimize the performance of the machine learning (ML) model, a binary FO approach was chosen for assessment on the 21^st day after IS onset: mRS ≥ 3 scores corresponded to an unfavorable non-lethal outcome, and mRS = 0–2 scores corresponded to a favorable FO. We analyzed the interrelation with FO (correlation coefficient, r) and the predictive ability (ML (decision tree), information gain, i. g.) of 29 parameters, including demographic features; comorbidities; instrumental examination findings; NIHSS, BI, CDR scores; serum concentrations of cytokines on the 2^nd day of hospital stay.

Results. The following significant (P<0.0001) predictors of unfavorable non-lethal FO were identified: female sex (i. g. = 0.346), recurrent IS (i. g = 0.248), diabetes mellitus (i. g. = 0.442), and CXCL2 concentration (i.g. = 0.306) in Group 1; WMHs severity (i. g. = 0.206), diabetes mellitus (i. g. = 0.340), content of CCL2 (i. g. = 0.116), CCL3 (i. g. = 0.202) and CCL23 (i. g. = 0.101) in Group 2; age (i. g. = 0.106), 2^nd –3^rd degree obesity (i. g. = 0.150), WMHs severity (i. g. = 0.300), CXCL5 content (i. g. = 0.143) and MIF (i. g. = 0.145) in Group 3. Concentrations of CCL25 (i. g. = 0.108) and IL-6 (i. g. = 0.401) were found as predictors of favorable FO (P<0.0001) in Group 1; 1^st degree obesity (i. g. = 0.118) and TNF-α concentration (i. g. = 0.211) in Group 2; arterial hypertension (AH) (i. g. = 0.113) and 1^st degree obesity in Group 3.

Conclusion. Study results made evident the variances in combination of factors affecting FO, depending on IS pathogenetic subtype. Despite undoubtful value of the data obtained, further research is needed to expand the potentiality in predicting acute IS outcome and confirm the relevance of identified markers.

The aim of the study was to identify the most specific and sensitive criteria for diagnosing nosocomial meningitis and ventriculitis.

Materials and methods. A retrospective case-control cohort study conducted at the department of anesthesiology and intensive care of the A. L. Polenov Russian Research Neurosurgical Institute (RRNI), a branch of the V. A. Almazov National Medical Research Center (NMRC) of the Ministry of Health of Russia included 120 patients who underwent intracranial neurosurgery: the main group (N=60) — patients with nosocomial meningitis (NM), and the comparison group (N=60) — patients without NM. Inclusion criteria: age over 18 years. Exclusion criteria: severe immunosuppressive condition (HIV infection), signs of central nervous system (CNS) infection (meningitis, ventriculitis, brain abscess) on admission, extracranial surgical interventions, pre-operative cerebrospinal fluid leakage, CNS trauma, and extracranial causes of CNS infection. The US Centers for Disease Control and Prevention (CDC) and the Burdenko National Medical Research Center for Neurosurgery criteria for NM diagnosis were used in the study.

Results. External validation of the NM diagnostic criteria in the analyzed patient cohort resulted in 81.67% sensitivity and 83.33% specificity of the CDC criteria. Sensitivity and specificity of the Burdenko National Medical Research Center for Neurosurgery criteria were 81.67% and 88.33%, respectively, for probable NM, and 51.67% and 100%, for confirmed NM. The CDC criteria demonstrated the highest sensitivity for protein concentration in cerebrospinal fluid (CSF) > 0.33 g/L (83.6%), with simultaneous extremely low specificity of 21%, and the highest specificity for the CSF positive culture (100%). As for the Burdenko National Research Medical Center for Neurosurgery criteria, in probable NM the highest sensitivity was established for CSF cell count > 65 cells/µL (64.4%), and the highest specificity — for CSF glucose < 2.6 mmol/l (93.9%) and CSF/serum glucose ratio (CSF/SGLU) < 0.45 (96.8%). In confirmed NM, CSF cell count > 65 cells/µL was also the most sensitive parameter (95.2%), although with 51% specificity. The highest specificity was found for the CSF lactate >

4.2 mmol/L (92.3%). The optimal threshold values were calculated for four parameters: body temperature

> 37.7°C, CSF cell count > 245 cells/µL, CSF glucose < 2.0 mmol/L, and CSF lactate > 3.7 mmol/L. Using a combination of threshold values for all four parameters, we achieved a sensitivity of 90.00% and a specificity of 91.67%. CSF cell count (AUC=0.90; 95% CI 0.84–0.95), increased CSF lactate (AUC=0.85; 95% CI 0.75–0.93), total CSF protein (AUC=0.83; 95% CI 0.75–0.90) and body temperature (AUC=0.82; 95% CI 0.74–0.89) had the greatest diagnostic value. Positive CSF culture and the occipital muscle rigidity correlated with the diagnosis of NM (rbp=0.522 and rbp=0.415, respectively, P=0.0001), but did not show good predictive diagnostic capacity.

Conclusion. Fever, increase in CSF cell count and CSF lactate were identified as the most clinically significant signs of NM. A positive CF culture traditionally used as the gold standard for diagnosis of NM showed low sensitivity of 69.2%. When taken together, the identified in the study threshold values of body temperature, CSF cell count, CSF glucose and lactate have a higher sensitivity and specificity than those used earlier.

The aim of this study was to investigate the effects of three 60-minute inhalations of an argon-oxygen gas mixture (Ar 70%/O₂ 30%) on the severity of neurological deficits, brain lesion volume, inflammatory and cellular responses, and cytokine levels in rats after photochemically induced ischemic stroke.

Materials and Methods. The experiment was performed in 21 male Wistar rats (250–300 g) randomly assigned to three groups: (1) ischemia + N₂ 70%/O₂ 30% inhalation (ischemia group, N=10); (2) ischemia + Ar 70%/O₂ 30% inhalation (ischemia + iAr group, N=8); and (3) sham-operated animals (sham group, N=3). Neurological status was assessed over 14 days using the limb placement test. On day 14 post-ischemia, animals underwent magnetic resonance imaging (MRI), histological and immunohistochemical analyses, and RT-PCR using RNA extracted from the liquid homogenate of the entire brain to evaluate the relative levels of IL-1β, IL-6, and TNF mRNAs.

Results. Significant differences in limb placement test scores were observed between ischemia and ischemia + iAr groups on day 3 (7.3 [5.3; 10.4] vs. 9.9 [10.2; 13.2], P=0.045) and day 7 (8.0 [7.3; 9.2] vs. 10.0 [9.0; 11.5], P=0.027). MRI showed a significantly smaller ischemia volume in the ischemia + iAr group compared to the ischemia group (12.5 [8.5; 17.4] mm³ vs. 21.0 [17.5; 22.68] mm³, P=0.01). Pro-inflammatory cytokine levels were significantly lower following argon-oxygen inhalation: IL-1β — 205 [175.5; 247.5] in the Ischemia + iAr group vs. 328.5 [299; 347.5] in the Ischemia group (P=0.001); TNF — 110.5 [93.5; 113] vs. 149.5 [126.5; 176.5], respectively (P=0.001).

Conclusion. Repeated 60 min inhalation of argon-oxygen mixture (Ar 70%/O₂ 30%) after photochemically induced ischemic stroke significantly reduces neurological impairment, modulates pro-inflammatory cytokine levels, and affects inflammatory and cellular responses.

Aim: to investigate the neuroprotective properties of lithium chloride in a rat model of open traumatic brain injury (OTBI).

Materials and Methods. An open traumatic brain injury (OTBI) model was induced using the D. M. Feeney method. The study included 40 male Wistar rats divided into four groups: sham-operated animals (sham, N=10); a OTBI control group (control, N=10); a group receiving lithium chloride at a dose of 1.5 mmol/kg after OTBI (OTBI + lithium 63 mg/kg, N=10); and a group receiving lithium chloride at a dose of 0.5 mmol/kg after OTBI (OTBI + lithium 21 mg/kg, N=10). Cognitive and neurological functions were assessed using the Morris water maze and the forelimb placing test. Brain lesion volume was assessed by magnetic resonance imaging (MRI) on day 14 post-injury.

Results. Lithium chloride at 63 mg/kg administered 60 minutes after OTBI reduced brain lesion volume by 41.5% compared to the control group (P=0.001), while the 21 mg/kg dose reduced lesion volume by 27.5% (P=0.001). Lithium chloride at 63 mg/kg improved cognitive performance by 71% compared to the control group (P=0.009); the 21 mg/kg dose resulted in a 65% improvement (P=0.010).

Conclusion. Lithium chloride at doses of 21 mg/kg and 63 mg/kg has neuroprotective properties, significantly reduces brain lesion volume (as confirmed by MRI), alleviates neurological deficits, and thereby improves cognitive function in animals after OTBI.

Ischemic stroke is currently considered as one of the most pressing public health issues. Despite the differences in underlying mechanisms of ischemic and ischemic-reperfusion damage to the nervous tissue, the ultimate percentage of disability depends on intervention effects on the penumbra zone. The use of dicholine succinate (DCS), a neuronal insulin-sensitizer, is a promising pharmacological agent for management and prevention of stroke consequences.

The aim of the study was to investigate the effect of pharmacological preconditioning with DCS on brain cell death in experimental ischemic stroke in rats.

Materials and methods. Ischemic stroke in rats (N=16) was modeled by injecting the vasoconstrictor endothelin-1 (ET-1) into the striatum. The effect of pharmacological preconditioning with DCS as the active substance was evaluated by measuring the area of brain infarction in brain sections stained with cresyl violet. The effect of DCS on glycolysis and oxidative phosphorylation in primary cultures of rat cerebellum cells was assessed by measuring the rate of extracellular acidification and the rate of oxygen uptake, respectively.

Results. DCS administration in the preconditioning mode for 7 days, once a day orally, at a dose of 50 mg/kg, reduces the maximum area of the brain infarction zone by 34% (P<0.05) compared to the control in the subsequent experimental ischemic stroke induced by ET-1 administration. Three-day incubation of rat cerebellum primary culture with 50 µM DCHS does not affect the basal levels of glycolysis (P=0.916) and cellular respiration (P=0.8346), but increases cellular glycolytic reserve by 70.0% (P<0.0001) compared to the control.

Conclusion. For the first time, the neuroprotective effect of pharmacological preconditioning with the neuronal insulin-sensitizer DCS in ischemic stroke has been shown. Mechanism of DCS action associates with an increase in the glycolytic reserve of brain cells, i.e., with increased ability of preconditioned cells to produce ATP and lactate via glycolysis in case of acutely compromised oxidative phosphorylation.

Objective: to clarify the pathogenesis of ischemic stroke in infectious diseases of the lower respiratory tract.

Material and methods. We searched the PubMed database for original research articles, clinical reports, review articles, editorials, commentaries, and short communications published before June 25, 2025. Additional studies that were not captured through the primary database search were analyzed after manually examining the reference lists of the selected articles. Articles were selected based on the relevance of the title and abstract to the purpose of this review. Data from 160 sources were included in the analysis.

Results. We have identified and analyzed in detail the mechanisms of ischemic stroke development in respiratory infections: activation of the coagulation system and disruption of natural anticoagulant and fibrinolytic mechanisms (1); interaction of the hemostasis system with innate immunity (2); the effect of infectious agents on the progression of atherosclerosis and the stability of the atherosclerotic plaque (3); the formation of thromboemboli in the pulmonary veins (4).

Conclusion. Both bacterial and viral infections can initiate a procoagulant state mediated by tissue factor, von Willebrand factor, platelet activation, neutrophil extracellular traps and decreased activity of endogenous anticoagulants. The infectious process localized in the lungs, characterized by damage to the pulmonary vascular endothelium, alveolocytes, intraalveolar fibrin deposition, edema, cellular infiltration, in concert with hemostasis alterations create conditions for the formation of thrombi in the pulmonary vessels. Thus, the pulmonary veins and venules can be a source of cerebral thromboembolism. This mechanism of thromboembolic stroke development largely explains causes of acute cerebrovascular events in patients with lower respiratory tract infection without cardiovascular risk factors. Another mechanism of ischemic stroke is associated with direct or indirect effects of pathogens on the stability of atherosclerotic plaques in cerebral vessels, which, together with systemic procoagulant imbalance, leads to the formation of atherothrombosis. Given the significant pathogenetic relationship between acute infectious lung diseases and cardioembolic and atherothrombotic strokes, clinical alertness regarding acute cerebrovascular events should be included in monitoring and management of such patients.

Aim: to explore the pathophysiological mechanisms and clinical significance of delta rhythms (≤4 Hz) in disorders of consciousness (DOC), including coma, unresponsive wakefulness syndrome (UWS), and minimally conscious state (MCS), as biomarkers for diagnosis, prognosis, and therapeutic targeting.

Materials and Methods. A narrative review was conducted, focusing on experimental and clinical findings related to delta rhythm generation and modulation in the disorder of consciousness (DOC). Emphasis was placed on thalamo-cortical interactions, cortical inhibition, neuromodulatory deficits, and the role of glial cells, neuroinflammation, and metabolic disruptions. Quantitative EEG analysis and advanced neuroimaging were highlighted as key tools for assessing delta activity.

Results. Delta rhythms were found to dominate EEGs across DOC states, with high-amplitude global activity in coma and low-amplitude activity in UWS, indicating cortical suppression and thalamocortical disconnection, respectively. In MCS, reduced delta power and improved connectivity correlated with intermittent purposeful behavior. Therapeutic interventions, including TMS, tACS, and pharmacological agents, showed potential for modulating delta rhythms. Additionally, stochastic resonance emerged as a novel mechanism to stabilize neural networks through noise.

Conclusion. Delta rhythms serve as crucial biomarkers in DOC, offering diagnostic, prognostic, and therapeutic value. Multimodal approaches that integrate EEG, neuroimaging, and mechanistic studies are essential for deepening understanding and improving clinical outcomes in DOC management.