Vol 19, No 3 (2025)

Introduction. The high prevalence of post-COVID syndrome (PCS), which frequently manifests with emotional disturbances, cognitive impairment, and asthenia, necessitates effective rehabilitation methods. One potential approach is electroencephalography (EEG)-based biofeedback (BFB) therapy, though its use in PCS management has been explored in only a few studies to date.

The study aimed to evaluate the effects of EEG α-rhythm BFB training on emotional state and cognitive function recovery, and reduction of astheniа symptoms in PCS patients.

Materials and methods. Patients diagnosed with U09. Post-COVID-19 condition were randomly assigned to two groups of 10 participants each. The main group underwent 12–15 sessions of EEG α-rhythm BFB training using the NeuroPlay-6C headset with the Neurocorrection of COVID-19 Psychoemotional Consequences protocol, while the control group received identical training without biofeedback. Assessments performed before and after the intervention included: emotional state evaluation (State-Trait Anxiety Inventory [STAI], Short Health Anxiety Inventory [SHAI], Beck Depression Inventory [BDI], Psychological Stress Measure [PSM-25]), cognitive function assessment (Addenbrooke’s Cognitive Examination III [ACE-III], Schulte tables, Stroop test, Tower of London test, N-back test, 10-word memory test), assessment of asthenia (Multidimensional Fatigue Inventory [MFI]), and sleep quality evaluation (Insomnia Severity Index [ISI]).

Results. In both groups, the training resulted in a significant reduction of personal anxiety, psychological stress, depression, and asthenia. The main group additionally demonstrated decreased health-related anxiety and improved information retention parameters. Intergroup comparison revealed more pronounced dynamics in the main group: greater reduction of general fatigue manifestations, increased immediate word recall volume, and improved retention of verbal information in working memory. The proportion of patients transitioning to milder symptom severity levels on individual scales was comparable between both groups.

Conclusion. EEG α-rhythm biofeedback training can be implemented at the outpatient rehabilitation stage for PCS patients.

Introduction. Cerebrovascular disease (CVD) is a heterogeneous group of difficult-to-diagnose conditions in which hemorheological and hemostatic disorders significantly impact the risk of ischemic stroke (IS), as well as the prognosis and response to reperfusion therapy and preventive treatment. Laboratory thrombotic hazard markers, such as the thrombin-antithrombin III (TAT) complex, the plasmin-α2-antiplasmin (PAP) complex, thrombomodulin (TM), and the tissue plasminogen activator (tPA)/plasminogen activator inhibitor-1 (PAI-1) activity ratio, have not been adequately evaluated as predictors of different IS subtypes. Their potential role in acute IS has also not been determined.

Aim. The study aimed to evaluate the diagnostic and predictive value of primary thrombotic hazard markers in patients with CVD.

Materials and methods. The retrospective study included 91 patients with acute IS (45% of men; median age: 62 years). At admission, primary clinical parameters were assessed, including a National Institutes of Health Stroke Scale (NIHSS) score. Laboratory parameters and thrombotic hazard markers were also measured using an enzyme-linked immunosorbent assay. Three IS subtypes included large artery atherosclerosis (LAA)-related IS (n = 32), lacunar IS (n = 27), and hemorheological (small artery occlusion-related) IS (n = 32). The clinical outcomes were evaluated at day 10 using the NIHSS scale. A comparison group included patients with chronic CVD (n = 29; 34% men; median age: 55 years).

Results. The plasma levels of almost all study biomarkers differed significantly between patients with IS and chronic CVD, as well as between patients with different IS subtypes. Four of six markers (PAI-1, PAP, TAT, t-PA/PAI-1) were significantly associated with IS development, with TAT showing the strongest association (odds ratio: 4.78; 95% confidence interval: 2.70, 9.68). Linear regression models were used to evaluate the predictive value of thrombotic hazard biomarkers for IS outcomes, and TAT showed the most significant association in this case (p < 0.001). An analysis of the differential value of study biomarkers for different IS subtypes showed that PAI-1 was the most sensitive (0.969) marker for LAA-related IS, while t-PA/PAI-1 (0.99) and TAT (0.889) demonstrated high predictive value for lacunar IS.

Conclusion. Thrombotic hazard markers are a promising laboratory tool for evaluating IS risk and predicting functional outcomes and response to reperfusion therapy in patients with IS.

Introduction. Levodopa and other dopaminergic agents remain the cornerstone of pharmacotherapy for Parkinson’s disease (PD). Two enzymes play key roles in dopamine metabolism: catechol-O-methyltransferase and monoamine oxidase type B, encoded by the COMT and MAO-B genes respectively.

This study aimed at analyzing potential association between dopaminergic therapy response and carrier status of COMT (rs4680) and MAO-B (rs1799836) polymorphisms in patients with PD.

Materials and methods. The study included 96 PD patients at stages 2–3 on the modified Hoehn and Yahr scale. Most patients (n=64; 66.7%) received levodopa/carbidopa, with 40.6% on combined dopaminergic therapy. All patients underwent assessment of dopaminergic therapy effictiveness using the difference in motor deficit (calculated from part III of the Unified Parkinson’s Disease Rating Scale) between the worst and best states (%). COMT and MAO-B polymorhisms were detected by real-time polymerase chain reaction.

Results. Allelic analysis demonstrated that carriers of the COMT gene rs4680 G allele responded better to dopaminergic therapy than A allele carriers (p = 0.038) (43.78 ± 18.15% vs 38.53 ± 16.58%; p = 0.038). Among men, we found no significant differences in therapy sensitivity related to MAO-B (rs1799836) variants, while female CC genotype carriers demonstrated better treatment response than TC heterozygotes (35.45 ± 17.78% vs 55.16 ± 11.22%; p=0.019).

Conclusion. Our data suggest that in patients with PD, not only drug-induced dyskinesias and motor fluctuations, but also overall sensitivity to dopaminergic therapy may be associated with specific COMT and MAO-B polymorphisms.

Induced pluripotent stem cell (iPSC)-based models represent an innovative approach to studying the pathogenesis of inherited Parkinson’s disease (PD) at molecular and cellular levels. The ability to derive neurons, astrocytes, and microglia carrying SNCA gene mutations from iPSCs significantly advances our understanding of key metabolic disturbances in PD. Each specific type of SNCA gene mutation (A53T, A30P, triplications, duplications, etc.) exhibits individual effects on functional and biochemical characteristics of differentiated cells. These differences involve synaptogenesis, extramitochondrial oxygen consumption, and protein metabolism. The diversity of effects makes critical the selection of strictly defined iPSC lines depending on research objectives. The aim of this review is to examine metabolic features of brain cells derived from iPSCs with inherited PD associated with SNCA mutations, as well as the potential of using iPSCs to develop personalized in vitro models for understanding disease mechanisms. This approach will facilitate identification of new therapeutic targets and refinement of existing technologies for diagnosis and targeted therapy.

Huntington’s disease (HD) is an autosomal dominant progressive neurodegenerative disorder for which effective disease-modifying treatments have not yet been developed. Current diagnosis of HD relies on clinical criteria and genetic testing. However, neuroimaging plays a crucial role in differentiating HD with similar phenotypes and, most importantly, in objectively monitoring the neurodegenerative process, particularly during the development of disease-modifying therapies. Novel technologies and imaging protocols have significantly advanced neuroimaging capabilities in HD patients in recent years. This review presents a range of promising neuroimaging modalities (magnetic resonance morphometry, functional MRI, diffusion tensor imaging, positron emission tomography, etc.) that assess HD neurodegenerative patterns from multiple perspectives and clarify disease mechanisms and their correlation with clinical manifestations. Further development of these technologies is important not only for neurology but also for neuropharmacology and neurophysiology.

Status epilepticus (SE) is a severe complication of cardiac surgery for cyanotic congenital heart defects in children. SE significantly worsens neurological prognosis and increases the likelihood of fatal outcomes. In most cases, epileptic seizures and status epilepticus in intensive care unit patients lack clinical manifestations and are detected exclusively through electroencephalography (EEG). In this study, we present a series of clinical observations demonstrating the transformation of SE from clinical to electrographic manifestations during anticonvulsant therapy in children with cyanotic congenital heart defects during the postoperative period. We emphasize the critical importance of EEG in managing SE in pediatric intensive care settings.