Vol 17, No 1 (2023)

Introduction. Brain health and active longevity are affected by a number of stroke risk factors. We should identify their relative impact on the main subtypes of ischemic stroke (IS) in middle-aged and senior women to consider prevention and management strategies.

Objective. To assess prevalence of isolated and combined factors that may contribute with a high probability to development of the various IS subtypes in women aged 45–74 years.

Materials and methods. The study included 348 female patients aged 45–74 years including 145 inpatients with carotid IS (main group) from Neurology Department 2, the Research Center of Neurology, and 203 women with cognitive disorders due to the chronic cerebral ischemia (controls). To assess the impact of various risk factors on the main IS subtypes, we generated multivariate predictive models using logistic regression and the Wald test.

Results. Predictive modeling of atherothrombotic IS demonstrated that type 2 diabetes mellitus increases IS risk by over 5 times (odds ratio [OR] = 5.961; 95% confidence interval [CI] 1.102–32.257; р = 0.038); internal carotid artery stenosis, by 7 times (OR = 7.187; 95% CI 1.827–28.273; р = 0.005); history of transient ischemic attacks (TIA), by 61 times (OR = 61.442; 95% CI 7.673–491.998; р < 0.001); excessive alcohol intake, by 49 times (OR = 49,382; 95% CI 4.557–535.121; р = 0.001); and HTN severity, by 4 times (OR = 4.445; 95% CI 2.331–8.476; р < 0.001). Predictive modeling of cardioembolic IS demonstrated that post-infarction cardiosclerosis increases IS risk by over 118 times (OR = 118.025; 95% CI 5.210–2673.796; р = 0.003), atrial fibrillation, by 108 times (OR = 108.493; 95% CI 24.312–484.159; р < 0.001), history of TIA, by over 71 times (OR = 71.558; 95% CI 7.945–644.535; р < 0.001); and HTN severity, by over 3 times (OR = 3.957; 95% CI 2.069–7.566; р < 0.001). Predictive modeling of lacunar IS demonstrated that type 2 diabetes mellitus increases IS risk by 8 times (OR = 8.324; 95% CI 1.923–36.041; р = 0.005), history of IS, by over 8 times (OR = 8.99; 95% CI 1.772–45.598; р = 0.008); and HTN severity, by 7 times (OR = 7.139; 95% CI 3.491–14.599; р < 0.001).

Conclusion. We identified a number of risk factors that may contribute to the development of the main IS subtypes in middle-aged and senior women.

Introduction. The crucial role of neuro-vascular conflict (NVC) in trigeminal neuralgia (TN) is getting increasingly challenged. Microstructural changes can be assessed using fractional anisotropy (FA) in diffusion tensor images (DTI).

Objective. To evaluate usefulness of FA in brain MRI with DTI for TN lateralization assessment.

Materials and methods. The study included 51 patients with classical TN divided into two groups: neurosurgical intervention free, post radiofrequency ablation (RFA), and a control group (patients without facial pain). All the patients were tested for NVC with FIESTA (Fast Imaging Employing Steady State Acquisition) brain MRI at 3Т. Difference in thickness of trigeminal roots on the intact and symptomatic sides was assessed for each group. The findings were compared to those in the control group. The MRI protocol was supplemented with DTI. The FA difference in thickness of the intact and symptomatic roots (∆FA) was calculated for each study group to assess microstructural root changes. The results were compared to those in the control group.

Results. In trigeminal root DTIs, ∆FA over 0.075 [0.029; 0.146] is statistically significant to establish NVC-associated microstructural changes on the symptomatic side in patients without any past surgeries (p = 0,030). In patients with a history of trigeminal ganglion RFA, statistically significant (p = 0.026) thinned symptomatic trigeminal root (difference in thickness of trigeminal roots over 0.45 cm [0.4; 0.6]) was found as compared to that of the control patients.

Conclusion. ΔFA may be used as a quantitative demyelination biomarker in clinical TN. Trigeminal ganglion RFA leads to hypotrophy throughout the trigeminal nerve root.

Introduction. Parkinson's disease (PD) urges for new instrumental methods of diagnosis. Transcranial sonography of the substantia nigra (SN TCS) is an established method for early PD diagnosis but its application is limited. Recently, biopsies (primarily that of salivary gland) and test for abnormal α-synuclein are suggested to verify PD.

Materials and methods. We assessed 12 individuals with PD, Hoehn–Yahr 2.3 ± 0.4. The assessments included: UPDRS, NMSQ, NMSS, RBDSQ, PDQ-8, MoCA, and HADS scoring; SN TCS; and sublingual gland immunohistochemistry for phosphorylated α-synuclein (PS-129) with automated morphometric analysis.

Results. Substantia nigra hyperechogenicity was shown in 75% of patients whereas biopsy revealed PS-129 in 100% of patients. Echogenic area of the substantia nigra was 0.24 [0.21; 0.3] cm². PS-129 inclusion area varied from 28.47 [27.55; 96.26] to 238.77 [234.13; 272.49] μm², and PS-129 proportion varied from 13.4% to 93.4% of the nervous fiber area across the patients. We found relations between PS-129 and NMSQ (r = 0.8; p < 0.001), NMSS (r = 0.9; p < 0.001), PDQ-8 (r = 0.7; p = 0.003), UPDRS-I (r = 0.7; p = 0.009), UPDRS-II (r = 0.6; p = 0.03), and HADS (anxiety r = 0.8; p = 0.002; depression r = 0.6; p = 0.04) scores.

Conclusion. The results demonstrate a higher biopsy sensitivity as compared to SN TCS. Automated morphometric analysis has been newly applied to assess PS-129 occurrence. Immunohistochemistry results are directly related to non-motor symptom severity, which may indicate high probability of PS-129 presence and diagnosis confirmation in early disease.

As endovascular reperfusion advances and multimodal neuroimagimg is implemented, neuroprotection in ischemic stroke progresses to the next level. In the recent years, the focus of neuroprotection research has been gradually shifting towards the research of endogenous substances and their synthetic analogs. According to the available evidence, thyroid hormones (THs) and their metabolites are potentially effective neuroprotectors in brain ischemia.

Objective. To identify and classify TH neuroprotective effects in acute brain ischemia by analyzing contemporary data.

We studied and analyzed publications indexed in РubMed, SciElo, ScienceDirect, Scopus, Biomedical Data Journal, and eLibrary.

The molecular basis of TH effects includes genomic and non-genomic mechanisms aimed at mitochondrial activity regulation, neuro- and angiogenesis, axonal transport, cytoskeleton maintenance, and impact on ion channels as well as activation and expression of specific proteins. TH effects on the central nervous system can be classified into following clusters: influence on neuronal and glial metabolism, apoptosis modulation, neuroplasticity and angiogenesis, impact on hemostasis, and local and systemic immune response.

Conclusion. THs are multimodal and selective regulators of cellular processes that affect neuroplasticity and neuro-reintegration both in the brain ischemic zone and beyond it. Therefore, a promising research can cover THs and and their metabolites as cerebral cytoprotectors to improve functional outcomes of ischemic strokes.

Carotid atherosclerosis is a significant cause of cerebrovascular disease. However, with many candidate markers, precise assessment of its development and progression risks is still limited. This paper reviews state-of-the-art concepts of microRNA as an atherogenesis biomarker throughout various stages including endothelial dysfunction, cholesterol/lipid metabolism, inflammation, oxidative stress, angiogenesis regulation, and proliferation and migration of vascular smooth muscle cells. Based on the available literature, we have described most significant microRNAs for each stage characterized in brief. We have visualized interactions between microRNAs and validated target genes with MIENTURNET and suggest and justify a set of microRNAs for further pilot studies of carotid atherosclerosis.

Introduction. Central nervous system is one of the main targets in patients with HIV infection. Neurological complications in AIDS are primarily caused by opportunistic brain infections including toxoplasmosis as the most common one. Patients with cerebral toxoplasmosis are often hospitalized with diagnosed strokes, tumors, or encephalitis. At that, their HIV status may be unknown and their state severity often does not allow conducting the range of required examinations.

Materials and methods. We have described our experience in management of 6 patients admitted to the neurosurgery department with single toxoplasmosis foci and diagnosed brain tumors.

Results. HIV infection was initially known in 3 patients only. In 2 compensated patients, the diagnosis was confirmed via Toxoplasma IgG blood test. In 2 individuals, negative serological Toxoplasma reactions were followed by neuronavigationally controlled biopsies. A patient with an extensive perifocal edema and, as a result, dislocated midline structures underwent decompressive craniectomy and mass removal. One female patient, with an unclear diagnosis, was operated for a suspected brain tumor. After additional assessments (including 4 histologies to confirm cerebral toxoplasmosis), all the patients were transferred to the infectious disease hospital for specific treatment.