Vol 20, No 2 (2026)

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. 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. 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.

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. 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.

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.