Background. Epilepsy is one of the most common neurological disorders, affecting individuals of all ages. For patients meeting the criteria for drug-resistant epilepsy established by the International League Against Epilepsy (ILAE), surgery is the most effective treatment option. The success of surgical outcomes depends directly on the precise localization of the epileptogenic focus. Positron emission tomography combined with magnetic resonance imaging (PET/MRI) is a novel hybrid diagnostic modality that may improve detection of the epileptogenic zone in complex diagnostic cases, including patients with MRI-negative epilepsy. Detecting the area of 18F-fluorodeoxyglucose (18F-FDG) hypometabolism in the epileptogenic focus is traditionally based on visual analysis; quantitative analysis techniques for hypometabolism in the epileptogenic focus have not been standardized and remain a subject of scientific investigation. Aim: To determine the optimal calculation metric (uptake index) of quantitative standardized uptake value (SUV) for detecting the epileptogenic focus in patients with drug-resistant epilepsy using brain 18F-FDG PET/MRI. Materials and methods. We retrospectively analyzed data from hybrid 18F-FDG PET/MRI brain studies performed in 10 healthy volunteers and 19 patients with drug-resistant epilepsy in whom the localization of the epileptogenic focus identified on PET/MRI was confirmed by surgical resection or invasive video-EEG monitoring. Results. The greatest variability in quantitative SUVmax and SUVmean was observed in patients with focal cortical dysplasia (FCD), while moderate variability in semi-quantitative SUVmax and SUVmean was observed in patients with mesial temporal sclerosis (MTS). The smallest reductions in SUVmax were observed in patients with FCD and MTS; for these patients, the SUVmean parameter was the best for localizing the epileptogenic focus. Analysis of brain PET/MRI data from patients with MRI-negative and MRI-positive epilepsy revealed no significant differences in semi-quantitative 18F-FDG metabolism parameters. In the group of patients with temporal lobe epilepsy, lower SUVmax and SUVmean were recorded, which may reflect the normally observed lower 18F-FDG metabolism in the temporal lobes compared to the cortex of other brain regions. Conclusion. Statistical analysis of quantitative 18F-FDG metabolism parameters in the epileptogenic focus confirmed by invasive methods indicates that the SUVmean parameter is optimal for identifying hypometabolic areas suspicious for the epileptogenic focus, due to its lower standard deviations and more homogeneous values within the sample, particularly in patients with FCD and MTS.
Post-stroke cognitive impairment (PSCI) is a major complication of cerebrovascular disease, spanning from mild cognitive impairment to dementia. PSCI pathogenesis involves complex mechanisms, including neuroinflammation, oxidative stress, and neuronal apoptosis. Recent studies have identified lipoprotein-associated phospholipase A2 (LP-PLA2) as a key enzyme in vascular inflammation and atherosclerosis, both of which are closely linked to post-stroke cognitive decline. LP-PLA2 contributes to PSCI pathogenesis via several pathways: (1) promoting vascular injury and neurodegeneration via inflammatory lipid metabolites such as lysophosphatidylcholine; (2) impairing the blood-brain barrier, leading to increased permeability and amyloid-β accumulation; and (3) inducing calcium-dependent neuronal apoptosis through oxidized fatty acids like arachidonic acid. These processes reduce cognitive reserve and neuroplasticity, thereby accelerating cognitive decline in ischemic stroke survivors. In addition, elevated LP-PLA2 levels have been associated with recurrent vascular events and unfavorable neurological outcomes, suggesting a role in ongoing post-stroke inflammation. Persistent activation of vascular inflammatory pathways may exacerbate cerebral small vessel disease, white matter damage, and synaptic dysfunction, which are critical determinants of long-term cognitive performance. The interaction between vascular injury and neurodegeneration further highlights the importance of inflammatory mediators in PSCI progression. Given its pathophysiological relevance, LP-PLA2 holds promise as a diagnostic biomarker and a therapeutic target for mitigating cognitive deterioration after stroke.
Introduction. Therapeutic options for ischemic stroke (IS) are largely limited to reperfusion, underscoring the importance of exploring new approaches to neuroprotection and neurorepair. Thyronamines — endogenous derivatives of thyroid hormones — are a promising class of compounds with putative neuroprotective potential. Study aim: To evaluate the effect of a synthetic thyronamine analog (SA-T0AM) on the levels of brain damage markers in a rat model of experimental IS. Materials and methods. The study was performed on 30 male Wistar rats divided into 4 groups: 1) Experimental — induction of focal cerebral cortical ischemia by application of ferric chloride followed by SA-T0AM administration; 2) Control — induction of ischemia without subsequent therapy; 3) Sham operation — all surgical manipulations except application of ferric chloride (0.9% NaCl solution was used); 4) intact animals. On day 3, concentrations of neuroglobin (NGB), glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF), neuron-specific enolase (NSE), and S100B protein were determined in the cerebral hemisphere tissue by enzyme-linked immunosorbent assay (ELISA). Results. Induction of ischemia led to a significant increase in the levels of all studied damage biomarkers in both hemispheres. Surgical intervention (craniotomy) caused a nonspecific increase in GFAP, NSE, and BDNF in all operated groups compared to intact animals. The key difference between the Experimental and Control groups was found in the non-ischemic hemisphere: administration of SA-T0AM was associated with a statistically significant increase in NGB content. Conclusion. The observed selective increase in NGB levels in the contralateral hemisphere following SA-T0AM administration indicates the compound’s ability to activate endogenous neuroprotective mechanisms in response to ischemic injury. This effect may be indirect or it may represent an independent direct action of the agent on neuroglobin expression, which requires further investigation. Although no intergroup differences were found for other brain damage markers (GFAP, NSE, S100B), which may be due to insufficient model sensitivity, the data suggest that further study of SA-T0AM is warranted as a pharmacological postconditioning agent in cerebral ischemia.
The article presents a global problem in modern neurology: post-stroke dysphagia. The anatomy, physiology, and pathophysiology of swallowing are presented. The prevalence and risk factors of post-stroke dysphagia are shown. The main complications that develop in patients with post-stroke dysphagia are described. The article presents the main diagnostic and therapeutic approaches for ensuring timely prevention and treatment of this serious complication in patients with strokes.
Introduction. Intraoperative neurophysiological monitoring is as crucial for preserving trigeminal nerve function during vestibular schwannoma (VS) resections as it is for monitoring facial nerve function. Study aim: To analyze the intraoperative reproducibility of the blink reflex (BR), assess its relationship with transcranial corticobulbar motor evoked potentials (CoMEP) and electromyographic monitoring data during VS removal, and determine its association with postoperative trigeminal nerve function. Materials and methods. The results of surgical treatment in the neurosurgery department of the Interregional Clinical Diagnostic Center in 2024–2025 were retrospectively analyzed for 17 patients with VS in whom BR was recorded intraoperatively. Standard modalities of intraoperative monitoring were studied: spontaneous and triggered electromyography, CoMEPs, somatosensory evoked potentials from the median nerve bilaterally, and electromyography of the masseter and temporalis muscles. Results. Intraoperatively, BR was reliably recorded in 82% of patients prior to VS removal. In patients with severe preoperative impairment of the trigeminal and facial nerves, BR was not detected intraoperatively. However, in 1 patient with significant deficits of the V and VII cranial nerves, BR was identified intraoperatively. In 3 (8%) patients, an abrupt loss of BR was recorded during monitoring. In 2 of these patients, the amplitude of CoMEPs decreased simultaneously; in 1 patient the decrease was critical, in another by 40%, and in 1 patient the CoMEPs remained stable. In cases of an acute loss of BR, patients developed sensory changes in the ipsilateral half of the face in the postoperative period. Conclusion. The method of BR recording during VS resection may become a valuable addition to intraoperative monitoring of CoMEPs and electromyography.
Introduction. Spinocerebellar ataxias lead to severe disability and impose a significant burden on healthcare systems. Experimental models are indispensable for reproducing the behavioral manifestations of ataxia and investigating novel therapeutic approaches; however, they do not fully replicate the entire spectrum of disease symptoms. Combined models are the most promising, as they more accurately reflect the complex pathogenetic mechanisms of neurodegeneration. Study aim: To assess the representativeness of the spinocerebellar ataxia phenotype model following combined exposure to lipopolysaccharide (LPS) and 3-acetylpyridine (3-AP) using behavioral tests. Materials and methods. The study was conducted on male Wistar rats (n = 30), randomly assigned to 4 groups. Animals in the Control+LPS and LPS+3-AP groups received LPS (40 μg in 10 μL) via bilateral intracerebroventricular (ICV) injection; rats in the Control and PS+3-AP groups received an equivalent volume of physiological saline. Three days later, animals in the PS+3-AP and LPS+3-AP groups received intraperitoneal injections of 3-AP (40 mg/kg); the Control and LPS+PS groups received physiological saline. The development of motor impairments was assessed using behavioral tests. Immunohistochemical methods were used to identify Purkinje cell (aldolase C) and microglial (IBA1) markers on cerebellar sections. Results. Body weight significantly decreased following combined exposure (p 0.01) and 3-AP alone (p 0.05), but not following LPS alone (p 0.05). Motor function impairments were significant in the LPS+3-AP and Control+3-AP groups (p 0.05). In the Control+LPS group, only isolated parameters showed significant changes compared to controls. Qualitative morphological analysis revealed more pronounced Purkinje cell dystrophy and microglial activation following combined exposure. Conclusion. Combined exposure to LPS and 3-AP reproduces a more pronounced ataxic phenotype, indicating a possible sensitizing effect of neuroinflammation and supporting the utility of this model for further investigation of this process.
Introduction. Divozilimab, a humanized, afucosylated monoclonal antibody that targets CD20, has been approved to treat multiple sclerosis, neuromyelitis optica spectrum disorders (NMOSD), and systemic sclerosis. The AQUARELLE clinical trial evaluates the efficacy and safety of divozilimab in patients with NMOSD. Aim. The study aimed to evaluate the efficacy and safety of divozilimab during the first year of treatment in patients with NMOSD. Materials and methods. The AQUARELLE open-label clinical trial enrolled 105 patients with NMOSD. All patients received 500 mg of divozilimab via intravenous infusion every 24 weeks. After 1 year of treatment, the following key parameters were evaluated: the annualized relapse rate (ARR), time to first relapse compared to a historical control group (the placebo group from the SakuraStar study), the proportion of patients with confirmed disability worsening (CDW), changes in Expanded Disability Status Scale (EDSS) scores, and safety parameters. Results. The ARR in patients with NMOSD who received divozilimab for one year was 0.104 (95% confidence interval [CI], 0.056–0.193), and 90.5% of patients had no confirmed relapses. The calculated weighted ratio of ARR (90% CI) for divozilimab to the historical placebo (SAkuraStar) was 0.237 (90% CI: 0.084–0.672), demonstrating superiority of divozilimab. The EDSS score remained stable, and no cases of CDW were reported. Adverse events (AEs) were observed in 76% of patients, most of which were mild or moderate in severity. The most common adverse drug reactions were lymphopenia (21%), leukopenia (11.4%), neutropenia (12.4%), and infusion-related reactions (5.7%). No serious adverse reactions were reported. Conclusion. The 1-year interim results of divozilimab therapy in patients with NMOSD from the AQUARELLE clinical trial demonstrate the sustained efficacy of therapy in reducing both the rate and risk of NMOSD relapses. Additionally, the safety profile was consistent with that expected for anti-B-cell therapy.
Introduction. Postanoxic encephalopathy (PAE) in children is a rare clinical condition characterized by movement disorders and decreased level of consciousness. The severity of clinical manifestations does not allow for defining a prognosis for the recovery of lost functions based solely on the results of the clinical examination and necessitates a comprehensive neurophysiological and neuroimaging screening, the scope and timing of which are undefined. The relationship between the child’s age at the time of hypoxic injury and the central nervous system ability to restore voluntary motor function has not yet been established. Study aim: To assess the structural and functional integrity of corticospinal and thalamocortical projections in children with PAE and to identify the leading diagnostic markers for predicting clinical outcomes regarding the restoration of voluntary motor function, taking into account the patient’s age at the time of injury. Materials and methods. The study included the results of follow-up assessment of 12 children with PAE aged from 1 to 16 years over the first year after injury. Clinical and instrumental examination included assessment of motor function, level of consciousness, presence of paroxysmal motor phenomena, somatosensory evoked potentials upon median nerve stimulation, video-electroencephalographic monitoring, single-pulse transcranial magnetic stimulation, brain structure morphometry; magnetic resonance tractography of the corticospinal tract (CST) from the primary motor cortex and supplementary motor area, visual assessment of the severity of atrophic brain changes with a focus on the CST and subcortical structures involved in voluntary motor function. Results. The clinical patter of movement disorders and decreased level of consciousness in children with PAE included generalized dystonias in 50% of cases. Myoclonus was recorded only in the younger age group in children with an unfavorable clinical outcome. Improvement of neurological symptoms was more pronounced in the intermediate period of the disease. Neurophysiological and neuroradiological predictors of a favorable PAE outcome, considering the age-dependent concept of locomotor act formation in our study, were: in children aged 6 years — cortical components of somatosensory evoked potentials (≥ 4 points on the Houlden grading system), physiological sleep patterns, and a dominant rhythm according to video-electroencephalographic monitoring (in the intermediate period of the disease). In children aged 6–16 years, in addition to the parameters described above, unchanged threshold of the evoked motor response or central motor conduction time and ≤ 5 points on the scale for assessing the severity of atrophic changes in the CST and subcortical structures involved in voluntary movement function on magnetic resonance imaging were considered. In a 14-year-old child with a partially preserved CST but total damage to the thalamocortical afferentation, voluntary movement function did not recover. Conclusion. The data indicate the importance of preserving the afferent component of the central nervous system in children with PAE across all age groups and also create a prerequisite for developing recommendations on the scope and timing of investigations depending on the child’s age. The period of locomotor act formation is associated with low diagnostic value of neurophysiological and neuroradiological methods for assessing the anatomical and functional integrity of the CST. Confirmation of the obtained results requires studies with a larger number of clinical observations followed by statistical data processing.
Introduction. Gait disorders are a common and severe consequence of stroke, limiting patient autonomy and quality of life. A functional near-infrared spectroscopy (NIRS)-based brain–computer interface (BCI) represents a promising technology for restoring motor functions; however, its application in gait rehabilitation remains insufficiently studied. Study aim: To evaluate the clinical applicability and technical feasibility of an NIRS-based BCI technology combined with a pneumatic plantar support load simulator (pneumatic orthosis) as an adjunct to comprehensive motor rehabilitation in post-stroke patients. Materials and methods. Seventeen patients were enrolled in the pilot study, of whom 15 (median age 58.0 [47.0; 64.0] years, median time since stroke 6.0 [3.0; 9.0] months) completed a course of 7–13 (median 10 [9; 10]) training sessions with the NIRS-BCI–pneumatic orthosis technology in addition to a comprehensive motor rehabilitation program. Motor function was assessed using the Fugl–Meyer Assessment scale for the lower extremity, the 10-Meter Walk Test, and the Timed Up and Go test. Results. A total of 147 NIRS-BCI–pneumatic orthosis training sessions were conducted, with a total median exposure of 229 minutes per patient. The median BCI classifier recognition rate for patients’ mental states was 54.93% [53.10; 69.70]. The median of the maximum achieved recognition rates was 75.57% [67.54; 87.14]. Characteristic hemodynamic activation patterns were identified in motor and associative cortical areas. Following the course, statistically significant improvements were noted on the Fugl–Meyer Assessment scale (from 19.0 [16.0; 24.0] to 24.0 [20.0; 25.0] points; p = 0.001) and the Timed Up and Go test (from 17.61 [14.21; 22.34] to 16.06 [13.00; 17.41] s; p = 0.041), but not on the 10-Meter Walk Test (p 0.05). Most patients tolerated the procedures satisfactorily; two participants withdrew early. Conclusion. The clinical applicability and technical feasibility of the NIRS-BCI–pneumatic orthosis technology for post-stroke gait rehabilitation have been confirmed. Randomized controlled trials are required to assess its clinical efficacy.
Introduction. Localization of cerebral cortex function is essential in neurology, neurosurgery, and neurorehabilitation, and is a subject of study for brain–computer interface developers. The history of functional mapping spans more than 100 years. During this time, both invasive and noninvasive techniques have been developed; however, debate regarding their accuracy and reproducibility continues. The study aim is to provide a narrative review and critical evaluation of the various functional mapping technologies of the cerebral cortex used in neurosurgery and neurorehabilitation. Results. The analysis included invasive and noninvasive methods of the functional mapping of the cerebral cortex (FMCC): intraoperative electrical stimulation using a manually controlled stimulation probe; extraoperative electrical stimulation using invasive electrodes; navigated transcranial magnetic stimulation; functional electrocorticography based on γ-activity modulation; and functional magnetic resonance imaging. The practice of selecting tasks for non-motor mapping of the cerebral cortex and the Wada test for lateralization of cognitive functions are discussed. The specific features and applications of each method are described, along with the reasons for their limited diagnostic yield. Directions for clinical research and technological development in the field of FMCC are proposed. Conclusion. Electrical stimulation of the brain remains the clinical gold standard for invasive FMCC; however, this method has significant limitations. Advances in other techniques allow the application of FMCC to be extended to patients with diverse baseline clinical characteristics. Common directions for advancing FMCC include the development of stimulus materials based on current knowledge of cognitive functions and their mapping potential, taking into account the specific features of each technique. A promising direction for advancement in FMCC is not the search for a universal method, but rather the integration of technologies and the creation of multimodal, integrative solutions.
We present a case series of lumbosacral plexopathy associated with clinically (neruologically) signficant monoclonal gammopathy. The aim of this publication is to demonstrate an atypical (non-polyneuritic) pattern of peripheral nervous system involvement in patients with monoclonal gammopathy. Possible therapeutic strategies for this patient population and their potential efficacy are discussed. In patients with progressive unilateral or bilateral lumbosacral plexopathy common causes should be excluded and serum protein electrophoresis with immunofixation should be performed; if positive, the patient should be referred to an hematologic oncologist to rule out the onset of a lymphoproliferative disease.
Introduction. The study of morphometric and microstructural characteristics of the brain in patients with temporal lobe epilepsy (TLE) represents one of the most rapidly advancing areas of neuroimaging research. Study aim: To quantitatively assess changes in morphometric and microstructural parameters of gray and white matter in the brains of patients with TLE. Materials and methods. The study included 55 subjects (29 patients with temporal lobe epilepsy and 26 healthy controls) aged 22–64 years. All patients underwent brain MRI according to an epilepsy protocol and diffusion MRI (3 Tesla). Voxel-based morphometry was performed using the CAT12 module in MATLAB 2018. Modeling of 32 white matter tracts was conducted automatically in DSI Studio 2022 using the HCP842 atlas-based algorithm. Results. Patients with TLE showed significant gray matter volume reduction in 54 regions and white matter volume reduction in 23 regions. Conversely, white matter volume increase was observed in 6 regions. Subgroup analysis of different structural abnormalities (hippocampal sclerosis, focal cortical dysplasia, low-grade glioneuronal tumor, cavernoma, encephalocele) revealed gray matter volume increase in 9 regions and white matter increase in 1 region. Additionally, white matter volume increase was documented in 3 regions in patients with bitemporal discharges and in 2 regions with hippocampal sclerosis. Microstructural changes were detected bilaterally — both ipsilateral and contralateral to the epileptogenic focus. Some changes indicated enhanced microstructural integrity and compaction of myelin fibers. Conclusion. Patients with TLE exhibit not only morphometric and microstructural signs of degenerative changes in cerebral gray and white matter, but also markers of compensatory neuroplastic mechanism activation.
Aim. This review evaluated the effects of physical and breathing exercises on functional outcomes, respiratory capacity, and quality of life (QoL) in patients with myasthenia gravis (MG). A structured search was conducted in PubMed, Web of Science, and Google Scholar, complemented by manual citation screening. Eligible studies included intervention trials and observational reports in English or Indonesian. Seven eligible studies, mainly intervention-based, were identified addressing the effects of physical and breathing exercises in MG. Evidence showed benefits in muscle strength, functional capacity, QoL, and respiratory function, with breathing exercises helping prevent complications. Physical and breathing exercises provide significant benefits for patients with MG. Interventions such as aerobic exercise, resistance exercise, respiratory muscle endurance training, and inspiratory muscle training improve pulmonary function, functional capacity, and reduce dyspnea and fatigue, accompanied by increased peripheral muscle strength and QoL. The underlying physiological mechanisms include enhanced respiratory muscle strength, ventilatory efficiency, diaphragm activation, and neuromuscular adaptations that mitigate fatigability without exacerbating MG symptoms. Progressive resistance exercise further supports peripheral oxygenation and neuromuscular plasticity. From a safety perspective, structured exercise programs are proven safe in patients with stable MG, without causing clinical exacerbations or neuromuscular deterioration. Mild side effects are transient and rarely require medical intervention. Adherence levels are high, with dropout rates more often influenced by non-medical factors. Conclusion. Physical and respiratory exercise yield measurable improvements in respiratory capacity, functional outcomes, and QoL in patients with MG, supporting their role as an effective disease management component.
Introduction. Chemotherapy (CT) with platinum and taxane drugs often leads to chemotherapy-induced peripheral neuropathy (CIPN), which significantly impairs patients’ quality of life. CIPN is diagnosed based on symptoms and neurological examination, which underscores the need for objective biomarkers. Promising criteria for peripheral nerve damage are neurofilaments, in particular the light chain (NfL) and peripherin. NfL is released during axonal damage but is not specific to the peripheral nervous system. Peripherin, in contrast, is expressed exclusively in peripheral neurons and is considered a more specific marker; however, its detection is challenging. The aim of the study was to evaluate serum levels of neurofilament and peripherin using the ELISA method in patients with solid tumors undergoing CT. Materials and methods. The study included 66 patients with newly diagnosed solid tumors before starting CT with platinum or taxanes. Patients with known risk factors for polyneuropathy and those taking medications with neurotoxic effects were excluded. After treatment, 51 patients were examined. Neurological examination with assessment using the NCI-CTCAE and NDS scales, nerve conduction study (SRAR index, amplitude of the sural nerve action potential), and assessment of intraepidermal nerve fiber density were performed. Serum levels of NfL and peripherin were measured using ELISA before and approximately 4.5 months after CT. Preanalytical sample processing was standardized. Results. After the CT course all patients showed a significant increase in NfL levels (p 0.0003). The most pronounced increase in the indicator (~fivefold) was recorded in male patients (p 0.001) and in the group of patients with malignant neoplasms in the gastrointestinal tract (p = 0.001). The concentration of peripherin in all analyzed samples was zero, likely due to the low ELISA sensitivity. In patients with developed CIPN, the NfL level after treatment was significantly higher (p = 0.001); however, no prognostic value for predicting neuropathy was found (AUC = 0.526; p = 0.803). At the same time, a moderate negative correlation was found between the NfL level and the density of intraepidermal nerve fibers (r = –0.416; p = 0.012). No statistically significant association was found between NfL concentration and electrophysiological parameters (SRAR index and sural nerve action potential amplitude). Conclusion. NfL is a promising but insufficiently specific biomarker for monitoring patients with CIPN. The absence of a detectable level of peripherin by ELISA limits its clinical application and suggests the use of more sensitive analytical methods.
Introduction. Ischemic stroke (IS) in young adults remains an unresolved major medical, social, and demographic issue. In a quarter of cases of acute cerebrovascular events in young age their origin remains unknown (i.e., cryptogenic stroke). Obesity and its associated conditions are considered risk factors contributing to premature cerebro-metabolic disorders. Chronic non-specific inflammation (metabolic inflammation) is regarded as a potential key mechanism for vascular events in obesity, though its role in IS among obese individuals is not fully understood. Studying cytokine levels as primary markers of meta-inflammation will help assess its role in IS in young adults. The study aimed at evaluating the role of inflammatory mediators, biochemical and hemostatic statuses in young patients with IS of unknown etiology and obesity. Materials and methods. A prospective study included 66 patients aged 18–50 years with IS of unknown etiology, divided into two groups: subjects with obesity (body mass index (BMI) ≥30 kg/m2; n = 34) and subjects with normal BMI (18.5–24.9 kg/m2; n = 32). Anthropometric, blood chemistry (lipid profile — low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, glucose, C-reactive protein, uric acid, homocysteine), hemostatic (factors VIII, IX, von Willebrand factor (vWF), antithrombin III, protein C), and immune (tumor necrosis factor-α (TNF-α), interleukins-6, -8, -10) blood parameters were analyzed. Results. Significant differences were observed in key markers of chronic nonspecific inflammation among obese patients. Homocysteine levels (p = 0.0001), factors VIII (p = 0.024), IX (p = 0.003) and vWF (p 0.0001), antithrombin III (p = 0.0041), LDL cholesterol (p = 0.0382), HDL cholesterol (p = 0.0112), and uric acid (p = 0.0011) were significantly higher in obese patients. Sex stratification revealed that obesity significantly influenced triglyceride levels (p = 0.021 in men), LDL cholesterol (p = 0.0177 in men), HDL cholesterol (p = 0.0348 in men), uric acid (p = 0.0348 in men and p = 0.0229 in women), homocysteine (p = 0.0013 in women), vWF (p 0.0001 in both sexes), factor VIII (p = 0.0091 in men), factor IX (p = 0.0209 in women), and antithrombin III (p = 0.0048 in men). Similar changes were detected in inflammatory markers and proinflammatory cytokines (C-reactive protein, neutrophils, tumor necrosis factor-α, interleukin-8, -10) compared to patients with normal BMI. Conclusion. Adipose tissue-initiated chronic nonspecific inflammation plays a significant role in the IS of unknown etiology in young adults by initiating and exacerbating endothelial dysfunction, prothrombotic, and atherosclerotic changes.
Introduction. Wilson–Konovalov disease is associated with impaired intracellular transport of Cu2+, resulting in increased concentrations of unbound copper in the blood, its accumulation in various organs and tissues, primarily the liver, brain, kidneys, and cornea. The resulting excess Cu2+ ions in the brain leads to altered astrocyte morphology, enlarged microglia, edema of oligodendroglia, reduced neuronal count, and impaired permeability of microcirculatory vessels. The study aimed to determine how Cu2+ excess affects angiogenesis and nucleoli in cultured rat cerebral cortex endothelial cells (ECs). Materials and methods. Copper chloride was added to the culture medium of rat cerebral cortex ECs at concentrations of 50–300 μM for 24 hours. Angiogenesis in cultures was studied using cultured rat brain ECs and the Angiogenesis Assay Kit. Cell viability was assessed using the MTT test, and nucleoli were stained with acridine orange. Results. The effect of Cu2+ on cultured rat cerebral cortex ECs was examined. MTT assay of cultures showed reduced formazan production starting at Cu2+ concentrations of 100 μM in the culture medium, indicating decreased cell viability. At this same concentration, Cu2+ -induced impairment of angiogenesis was observed in EC cultures. At higher Cu2+ concentrations (200 μM), surviving cells exhibited a statistically significant increase in nucleolar size to 1.71 ± 0.09 μm2 compared to 1.33 ± 0.07 μm2 in control cultures. Conclusion. Thus, excess copper ions reduce angiogenesis and induce changes in ECs nucleoli, which may represent a universal cellular response associated with cell damage.
Introduction. The blood-brain barrier (BBB) is a component of the neurovascular unit and a system regulating chemical homeostasis in brain tissue. Assessment of BBB permeability under normal and abnormal states of the central nervous system is of significant interest for experimental research in neuroscience. In recent years, there has been a substantial expansion of protocols that can be used to address such research tasks. Understanding the key differences, advantages, and limitations of each BBB investigation method is crucial for proper experimental design and data interpretation. The aim of this review is to analyze modern methods for assessing BBB permeability in laboratory animals using fluorescent probes (tracers), provide their comparative characteristics, and evaluate selection criteria for solving experimental tasks. Conclusion. Fluorescent probes enable real-time monitoring of BBB status in vivo during experimental neuroscience studies when assessing structural and functional integrity of the barrier in neuroinflammation, neurodegeneration, and brain tissue injury. Proper selection of fluorescent probes allows differentiated evaluation of para- and transcellular BBB permeability, vascular wall structure, and processes associated with brain tissue clearance.
One of the key reasons for the high incidence of adverse outcomes in gunshot wounds to the head is the multifactorial damaging effect of high-energy projectiles. One complication of gunshot wounds to the neck or head is traumatic arteriovenous fistulas (AVFs). The cases of traumatic intracranial AVFs resulting from gunshot wounds to the head, involving the proximal segments of the internal carotid artery (ICA) or other major cerebral arteries are unique if they are accompanied by a favorable clinical outcome. Russian and foreign literature sources do not provide information on clinical observations of traumatic intracranial extradural AVFs. The article describes a clinical case of a patient with traumatic intracranial extradural carotid-jugular fistula resulting from a gunshot fragment through-and-through craniobasal wound to the head in the left occipital region, with a comminuted fracture of the occipital bone, a through-and-through fracture of the pyramid of the left temporal bone, a perforated fracture of the left greater wing of the sphenoid bone, an exit wound in the soft palate, and the formation of brain contusion foci along the wound channel. Clinically suspected and confirmed by ultrasound and computed tomographic angiographic studies of the brachiocephalic vessels, a traumatic carotid-jugular fistula was identified within the wound tract at the defect of the left temporal bone, combined with ICA occlusionat the C2 (petrous) segment, which did not lead to ischemic stroke on the affected side. Selective cerebral angiography was performed, followed by embolization of the left ICA stump in the cervical segment using detachable microcoils, achieving disconnection of the AVF. This case of traumatic carotid-jugular fistula is unique and demonstrates the possibility of a favorable outcome gunshot wound to the head due to timely diagnosis and endovascular intervention. The expediency of computed tomographic angiography for all patients with combat trauma to the head and neck is justified.
Hereditary transthyretin amyloidosis is a fatal systemic progressive disease caused by mutations in the transthyretin (TTR) gene, inherited in an autosomal dominant pattern, primarily affecting the peripheral and autonomic nervous systems and the heart, as well as the kidneys, liver, eyes, and gastrointestinal tract, leading to disability and a fatal outcome. The article presents a clinical case of hereditary transthyretin amyloidosis with predominant polyneuropathy manifestations in a 61-year-old male patient, caused by the most common variant of TTR gene mutation — the Val30Met mutation. An analysis and summary of the symptoms of transthyretin amyloidosis caused by the Val30Met mutation in the TTR gene, with early and late disease onset, were conducted.
We retrospectively analyzed data from 5 patients with a clinically established diagnosis of Parkinson’s disease (PD) who underwent positron emission tomography combined with computed tomography (PET/CT) of the brain using the 18F-DOPA radiopharmaceutical. The study included quantitative assessment of tracer uptake — SUVr in the anterior and posterior parts of the putamen, as well as visual assessment of asymmetry and hypometabolism patterns. In all clinical cases included in the analysis, we recorded a significant reduction in tracer uptake in the projection of the putamen compared to healthy controls, which directly reflects progressive loss of dopaminergic neurons. All examined patients exhibited patterns characteristic of PD: a posterior-to-anterior gradient of involvement (most pronounced reduction in SUVr in the posterior putamen) and asymmetry of nigrostriatal degeneration. The side with more pronounced reduction in tracer uptake was generally contralateral to the side with more severe clinical symptoms. In the patient with a PRKN gene mutation, marked, nearly symmetric reduction in tracer uptake was recorded.
