Aim. To summarize current evidence on the effects of cognitive training (CoTr) on cognitive function and brain reserves in cognitively intact individuals and patients with mild cognitive impairment (MCI) during aging.

Material and  methods. The authors searched the PubMed, Google Scholar, and eLIBRARY.RU databases for publications from 2018 to 2025 using combinations of Russian and English keywords: “cognitive training,” “brain reserve,” “brain networks,” “virtual reality,” “connectivity,” “healthy,” and “mild cognitive impairment.” The review included full-text studies assessing the isolated effects of CoTr on cognitive function and/or neurobiological indicators reflecting brain reserve in healthy individuals and patients with MCI. A total of 69 publications were included in the final analysis.

Results. CoTr programs were typically standardized and predominantly computerized, administered 2–5 times per week over 4–12 weeks. Training effectiveness was assessed using validated neuropsychological measures and neuroimaging techniques. Most randomized controlled trials provided evidence of statistically significant positive effects of CoTr on cognitive performance and brain parameters, with more pronounced benefits observed in cognitively healthy individuals than in patients with MCI. Associations were identified between CoTr-induced cognitive improvements in middle-aged and older adults and changes in functional connectivity of neural networks, cortical thickness, and microstructural integrity of cerebral white matter.

Conclusion. Cognitive training is considered a promising strategy for maintaining cognitive health. However, heterogeneity of existing training protocols and limited durability of effects indicate the need for further development of standardized and available cognitive exercise programs.

Spinal cord injury remains one of the most challenging medical and social issues, leading to long-term disability. Modern neuromodulation techniques provide new opportunities for motor function recovery, spasticity reduction, and neuropathic pain control; however, their effectiveness requires systematic evaluation.

Objective. To summarize current evidence on the use of functional electrical stimulation, transcranial magnetic stimulation, transcranial direct current stimulation, and transcutaneous spinal cord stimulation in patients with spinal cord injury.

Material and methods. A review of systematic reviews and meta-analyses published in international databases (PubMed, Scopus, Web of Science, eLibrary) between 2015 and 2025 was performed. A total of 35 sources, including results of randomized clinical trials and network meta-analyses, were analyzed.

Results. Functional electrical stimulation demonstrated a pronounced effect in improving respiratory function, endurance, and reducing spasticity. Transcranial magnetic stimulation contributed to motor function recovery, increased muscle strength, and reduced pain. Transcranial direct current stimulation showed moderate analgesic effects while maintaining a high safety profile. Transcutaneous spinal cord stimulation was effective in reducing spasticity and improving lower limb strength, particularly when combined with physical rehabilitation.

Conclusion. Non-invasive neuromodulation is a promising adjunct to standard therapy for spinal cord injury. It enhances motor function recovery, reduces spasticity and pain, and improves patients’ quality of life. Further highquality studies are needed before its integration into clinical practice.

The objective of the study was to analyze the clinical and laboratory factors in the acute period of ischemic stroke (IS) that predispose to the development of various manifestations of asthenia (pathological fatigue) 6 months later.

Material and methods. The data of 98 patients recruited in the acute period of IS and who agreed to a telephone interview 6 months later were analyzed. Post-stroke asthenia (PSA) was assessed using the subjective scale for assessing fatigue (MFI-20)). The severity of stroke (National Institutes of Health Stroke Scale (NIHSS), Rankin Scale, Rivermead Mobility Index), cognitive impairment, apathy, depression, anxiety, and laboratory and instrumental data obtained in acute period of stroke were registered. Linear regression analysis was performed to identify predictors of the severity of various manifestations of late-onset PSA.

Results. Cognitive decline was an independent predictor of the severity of general fatigue. The severity of stroke was a significant predictor of reduced activity and physical fatigue. Mobility impairment on the Rivermead scale was a predictor of decreased motivation. The severity of mental fatigue was associated with increased anxiety.

Conclusion. The data obtained demonstrate the clinical and pathogenetic heterogeneity of various manifestations of late PSA. This determines the need to develop differentiated approaches to the prevention of PSA.

Introduction. For decades, strokes have been a significant cause of disability and mortality in older populations worldwide. Characteristic features of this category of patients are the high prevalence of atherosclerosis of the brachiocephalic arteries, changes in the hormonal profile, progressive decrease in muscle tissue and increase in adipose tissue.

Objective of the Study. To study the frequency of occurrence of high-risk signs of atherosclerosis-associated cerebrovascular complications in the comorbid course of carotid artery atherosclerosis and sarcopenia.

Material and Methods. Two groups of patients over 55 years of age were examined (198 individuals with normal muscle mass and 69 with sarcopenia). The following assessments were performed: total cholesterol levels, ultrasound of brachiocephalic arteries, calculation of 10-year stroke risk (Framingham Risk Score), and 10-year mortality risk (SCORE scale). Group comparison was conducted using non-parametric statistical methods.

Results. Patients with sarcopenia showed a statistically significant higher incidence of carotid atherosclerosis and unstable atherosclerotic plaques. The Framingham and SCORE scores are insensitive to identifying high vascular risk in patients with comorbid atherosclerosis and sarcopenia.

Conclusion. Loss of muscle mass is associated with a higher incidence of multifocal atherosclerosis of the carotid arteries with signs of atherosclerotic plaque instability.

Background. Despite the positioning of duloxetine as a first-line agent for chemotherapy-induced neuropathy therapy, there are no direct comparative studies of its efficacy versus alternative medications, particularly considering the critically important factor of patient adherence to long-term treatment.

Objective. To compare the efficacy of duloxetine and thioctic acid in patients with chemotherapy-induced peripheral neuropathy (CIPN) with emphasis on treatment adherence.

Material and methods. A prospective randomized study included 59 patients (26 in the duloxetine group, 33 in the thioctic acid group). Efficacy was assessed using a battery of validated scales: Neurological Disability Score (NDS), Visual Analog Scale for pain (VAS), DN4 questionnaire for verification of neuropathic pain component (Neuropathic Pain Diagnostic Questionnaire, DN4). Safety was recorded according to the principles of Good Clinical Practice (International Council for Harmonisation — Good Clinical Practice, ICH-GCP). Adherence was evaluated by direct patient interviews at 1 month with registration of discontinuation reasons.

Results. Analysis of DN4 and NDS scores revealed no statistically significant differences. However, VAS showed a statistically significant difference (p = 0.02): pain increased in the duloxetine group (+ 0.94 ± 2.03 points) and decreased in the thioctic acid group (–0.11 ± 1.32 points). Adherence to duloxetine was 76.9% (20/26) versus 90.9% (30/33) for thioctic acid. Analysis of discontinuation reasons showed that in the duloxetine group, 83.3% of discontinuations were due to adverse effects and 16.7% to psychological barriers related to antidepressant positioning. Adverse effects were registered in 30.8% of duloxetine group patients and 9.1% of thioctic acid group (p = 0.07).

Conclusion. Given comparable objective efficacy and more favorable subjective pain dynamics in the thioctic acid group, adherence emerges as the key differentiating factor (76.9% vs 90.9%). The superior safety profile of thioctic acid and absence of psychological barriers make it the drug of first choice for long-term CIPN therapy.

Background. Wilson’s disease (WD) is characterized by wide phenotypic heterogeneity and may manifest not only in childhood and young adulthood but also after 40 years of age, which complicates timely diagnosis and worsens prognosis.

Objective. To analyze the clinical, genetic, laboratory, and neuroimaging features of neurological forms of late-onset WD.

Methods. Ninety-eight patients with neurological WD who were followed at a neurological research center from 2016 to 2025 were examined. In 16 patients (16.3%), disease onset occurred after the age of 40. A retrospective analysis of clinical manifestations, copper metabolism parameters, liver function tests, brain MRI findings at disease onset, and DNA diagnostic results was performed. The findings were compared with those in patients with a typical age of onset.

Results. In late-onset WD, tremor and tremor–rigid forms were observed more frequently, with a predominance of tremor and parkinsonian features. Disturbances of copper metabolism were less pronounced. Compensated liver cirrhosis predominated, and putaminal involvement on MRI was less frequent. Molecular genetic analysis revealed that the known pathogenic ATP7B variant p.H1069Q was more frequently detected in the homozygous state (68.8%).

Conclusion. Late-onset WD has a distinct neurological and radiological profile and may closely mimic common adult-onset movement disorders. WD should be routinely considered in the differential diagnosis of extrapyramidal syndromes, even in patients over 40 years of age.

The aim. To determine the level of ADMA in blood plasma and evaluate its role in the development of endothelial dysfunction in various pathogenetic subtypes of stroke in working-age men (18–50 years).

Material and methods. The study was conducted on a sample of 125 men (mean age 42.6 ± 5.3 years) with various subtypes of IS who were admitted to the neurological department before the COVID-19 pandemic. The study included 60 patients with atherothrombotic stroke (ATS), 46 patients with lacunar stroke (LS), and 19 patients with cardioembolic stroke (CES). The IS subtype was determined based on the TOAST classification (Trial of Org 10172 in Acute Stroke Treatment). The patients underwent risk factor assessment, detailed somatic and neurological examinations, neuroimaging of the brain, ultrasound examination of the main arteries of the head, and laboratory tests.

Results. In men aged 18–50 years with various subtypes of IS, the following risk factors were identified: arterial hypertension in 83.2%, dyslipidemia in 50.4%, diabetes mellitus in 8%, smoking in 67.2%, alcohol consumption in 29.6%, obesity in 16.8%, cardiac arrhythmia in 12%, a history of stroke in 16.8%, and a history of acute myocardial infarction in 10.4%. In men aged 18–50, the level of ADMA was higher in patients with ATS and LS compared to patients with CES. Patients with ATS had the highest levels of ADMA. Patients with ATS aged 41–50 had higher levels of ADMA compared to patients aged 31–40. Patients with LS and CES had higher levels of ADMA at the age of 31–40 years compared to patients aged 41–50 years. Significant correlations were found between the level of ADMA and individual risk factors in different subtypes of IS.

Conclusion. The identified changes in the level of ADMA and the obtained correlation relationships reflect the role of ADMA in the development and progression of atherosclerosis and endothelial dysfunction in men aged 18–50 with various subtypes of IS.

Background. Epilepsy is one of the most common neurological disorders of childhood, structurally comprising not only seizures but also a complex of cognitive, emotional, personality, and social impairments. Early identification of neurocognitive correlates is a key predictor of a favorable outcome; however, objective diagnosis of complex mental phenomena for children aged 1–3 years remains a methodological challenge.

Objective. To identify specific neurocognitive correlates of self-identification development for young children with epilepsy.

Material and мethods. The study involved 34 children (18 diagnosed with epilepsy and 16 normotypical children). A multimethodological approach was used, including: 1) an original hardware and software system (HSS) for assessing the level of self-identification development based on sensitivity to visual cues in one’s own image; 2) functional near-infrared spectroscopy (fNIRS) to record oxygenation (HbO) and deoxygenation (HbR) in the occipital lobes; 3) neuropsychological tests of facial gnosis; 4) the DP-3 general development questionnaire. The theoretical basis was I.L. Brandl’s concept of self-identification and A. R. Luria’s structural-functional model.

Results. It was established that in children with epilepsy, the process of self-identification development is nonlinear and quasi-periodic, in contrast to the progressive development in the control group. In children with epilepsy and unstable self-identification, significant differences in neurocognitive markers were found between all subgroups (in terms of sensitivity to 1, 2, and 3 PAC markers), whereas in healthy children, clear differentiation was observed only upon transition to a stable level. The most significant intergroup differences between children with epilepsy and healthy controls were found in the subgroup with the most developed self-identification (sensitivity to 3 markers) based on general development (DP-3) and oxygenation (HbO).

Conclusion. The preliminary results support the hypothesis that epilepsy most disrupts the final, integrative stages of self-identification development, disrupting the coordination of complex perceptual, cognitive, and affective components of the self. The identified specificity —nonlinearity and premature differentiation of neurocognitive profiles — substantiates the need to develop targeted neurorehabilitation programs aimed at supporting sensory integration and self-identification consolidation. Further extensive studies are needed to assess cognitive impairment depending on the form and course of the disease, including taking into account specific genetic forms of epilepsy and the drug therapy used.