Polycythemia vera (PV) is a Ph-negative myeloproliferative neoplasm (MPN) which is characterized by erythrocytosis and a high incidence of thrombotic complications, including stroke. The study aimed to evaluate red blood cell (RBC) morphodynamic properties in PV patients and their possible association with stroke. We enrolled 48 patients with PV in this cross-sectional study, 13 of which have a history of ischemic stroke. The control group consisted of 90 healthy subjects. RBC deformability and aggregation analysis were performed using a laser-assisted optical rotational red cell analyzer. The following parameters were calculated: aggregation amplitude (Amp), RBC rouleaux formation time constant (Tf), time of formation of three-dimensional aggregates (Ts), aggregation index (AI), rate of complete disaggregation (y-dis), and the maximal elongation of RBC (EImax). Statistical analysis was performed with the R programming language. There were significant differences in RBCs morphodynamics features between patients with PV and the control group. Lower EImax (0.47 (0.44; 0.51) vs. 0.51 (0.47; 0.54), p < 0.001) and γ-dis (100 (100; 140) vs. 140 (106; 188) sec−1, p < 0.001) along with higher amplitude (10.1 (8.6; 12.2) vs. 7.7 (6.6; 9.2), p < 0.001) was seen in patients with PV compared with control. A statistically significant difference between PV patients with and without stroke in aggregation amplitude was found (p = 0.03). A logistic regression model for stroke was built based on RBC morphodynamics which performed reasonably well (p = 0.01). RBC alterations may be associated with overt cerebrovascular disease in PV, suggesting a possible link between erythrocyte morphodynamics and increased risk of stroke.

Carotid atherosclerosis (CA) is an important risk factor for ischemic stroke. We described the miRNA and hemostasis profile of patients with moderate and advanced stages of carotid atherosclerosis and elucidated potential correlations with hemostatic activation. A prospective case-control study included 61 patients with evidence of carotid atherosclerosis (via ultrasound). The study population was divided into groups depending on the degree of carotid artery stenosis: 60% or more (advanced) and <60% (moderate). All patients underwent the following blood tests: general blood test, hemostatic parameters and microRNA. Extraction of microRNA was performed using Leukocyte RNA Purification Kit (NORGEN Biotec Сorp., Thorold, ON, Canada); miRNA quantification was performed via RT-PCR. Statistical analysis was performed in R programming language (v. 4.1.0) using RSudio. MicroRNA expression profile was different depending on CA degree. MiR-33a-5p/3p levels were higher in patients with ≥60% carotid stenosis (42.70 and 42.45 versus 38.50 and 38.50, respectively, p < 0.05). Almost complete separation can be visualized with the levels of miR-126-5p: 9.50 in the moderate CA group versus 5.25 in the advanced CA (p < 0.001). MiR-29-5p was higher in the moderate CA group: 28.60 [25.50;33.05] than in advanced CA group: 25.75 [24.38;29.50] (p = 0.086); miR-29-3p was also higher in the moderate CA group: 10.36 [8.60;14.99] than in advanced CA group: 8.46 [7.47;10.3] (p = 0.001). By-group pairwise correlation analyses revealed at least three clusters with significant positive correlations in the moderate CA group: miR-29-3p with factors V and XII (r = 0.53 and r = 0.37, respectively, p < 0.05); miR-21-5p with ADAMTS13, erythrocyte sedimentation rate and D-dimer (r = 0.42, r = 0.36 and r = 0.44, respectively, p < 0.05); stenosis degree with miR-33a-5p/3p and factor VIII levels (r = 0.43 (both) and r = 0.62, respectively, p < 0.05). Hemostasis parameters did not reveal significant changes in CA patients: the only statistically significant differences concerned factor VIII, plasminogen and (marginally significant) ADAMTS-13 and protein C. Down-regulation of miR-126-5p expression has been identified as a promising biomarker of advanced carotid atherosclerosis with high specificity and sensitivity. Correlation cluster analysis showed potential interplay between miRNAs and hemostatic activation in the setting of carotid atherosclerosis.

Traumatic trigeminal neuropathy occupies a special place in the pain continuum. The clarification of genesis and clinical and neurophysiological findings makes it possible to perform differentiation treatment.Objective: to evaluate the clinical and neurophysiological efficiency of repetitive magnetic stimulation (RMS) and vitamin B complex therapy for traumatic trigeminal neuropathy.Patients and methods. The investigation enrolled 36 patients (26 women and 10 men) aged 25 to 35 years with inferior alveolar neuropathy following bilateral sagittal split osteotomy. The DN4 questionnaire was used to identify a neurogenic pain component. The intensity of pain syndrome was assessed using a visual analogue scale. A neurophysiological examination involving the recording of brainstem auditory evoked potentials (BAEPs) and trigeminal evoked potentials (TEPs) was made using a Neuro-MEP device (Neurosoft, Russia). Therapy including vitamin B complex was performed in 12 patients. Twenty-four patients received low-frequency pulsed magnetic field therapy using a Neuro-MS magnetic stimulator.Results and discussion. The clinical picture in patients with traumatic inferior alveolar neuropathy after corrective mandible surgery is characterized by the polymorphism of pain sensations and sensory disorders. The development of pain syndrome is due to a neuropathic component. The 10-day vitamin group B therapy cycle had no substantial impact on the time course of clinical and neurophysiological changes. After the 10-day RMS cycle, there were reductions in swelling and the intensity of pain syndrome and the severity of sensory disorders in the lower lip, chin, and mandible. The data on BAEPs showed shortening in the interpeak intervals III–V; those on TEPs demonstrated a decrease in the P1–N1 amplitude.Conclusion. Unlike vitamin B complex therapy, the RMS cycle in patients with traumatic trigeminal neuropathy makes it possible to reduce the intensity of pain syndrome and the severity of sensory disorders, as well as excitability of the nonspecific structures of the brainstem and the central structures of the trigeminal system.

Background. Type 2 diabetes (Т2DM) both directly and indirectly impacts the development of morphological and functional changes of the central nervous system. Aim. The study was to determine clinical and neurophysiological patterns of cognitive impairment (CI) in patients with chronic cerebrovascular diseases (CCD) and Т2DM. Materials and methods. We examined 132 patients with CCD. First group included 58 patients without Т2DM aged 64.5 [58; 72], second group 74 patients with CCD and Т2DM 63 [57; 70]. Clinical, neurological, neuropsychological, neurophysiological (cognitive evoked potentials (EP) and neurovisualisation (brain MRI) examination was carried out to all patients. Results. Somatic and neurological characteristics of the patients were similar in both groups with the exception of more distinct metabolic changes in Т2DM patients. Neurovisualisation study of the brain MRI in Т2DM patients revealed more distinct changes in the form of white matter hyperintensity and subarachnoidal spaces enlargement. Neuropsychological examination in patients revealed the reduction of intellectual flexibility, constructive praxis disruption, optical spatial dysfunction and deteoration of delayed word recall. Significant disorders in the way of overall cognitive impairment, lobar dysfunction and impaired verbal associative productivity, proved by statistically lower amplitude and higher latency of P300 EP peak were noted in Т2DM patients. Correlation links were detected: for P300 amplitude and direct and inverse number listing test (r=0.366 and r=0.520; p=0.006 and p0.001 respectively); P300 latency and HbA1c (r=0.32; р0.05) in group 2 and glucose levels in both groups (r=0.30; p0.05); inverse relationship of latency with control functions evaluation (r=-0.34; p=0.008). Conclusion. CCD especially with Т2DM manifests with neurocognitive imbalance, including control functions disruption and are accompanied by neurophysiological and neurovisualistion changes.

Introduction: Neurology is arguably one of the most difficult subjects to teach and study in the medical curriculum. Educational games (EG) may be a valid option to enhance motivation in neurology residents.Methods: We developed an educational board game (Neuropoly) to assist in teaching neurology. We present here an overview of the game, as well as the results of a pilot study aimed at determining: (a) the efficacy of the game in teaching certain neurological concepts; and (b) student compliance and satisfaction with the EG.Results: The pre- and post-play questionnaire scores differed significantly (3.2 ± 1.7 vs. 7.8 ± 1.6, p &lt; 0.001). Our group of residents, showing an overwhelmingly positive response, very well received the game. The questions were rated as above average regarding difficulty.Conclusion: The “Neuropoly” educational board game has been shown to be interesting, efficient, and motivational among first- and second-year neurology residents. Novel educational methods for complex medical disciplines should be developed, with board games being a viable and inexpensive approach.

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