scholarly journals Experience in the application of non-invasive neuromodulation in the angioneurology

Author(s):  
Alexey A. Voropaev ◽  
Galina E. Ivanova ◽  
Tatiana V. Nikolaeva

The electromagnetic field is a fundamental factor of objective reality, when exposed to the brain causes the appearance and development of a complex of functional changes that help in the study of the properties of the nervous system itself. Non-invasive neuromodulation is a therapeutic exogenous effect on various parts of the nervous system (mainly vegetative) with the help of electromagnetic physical (electric, magnetic) factors in the course of drug therapy in accordance with the standards of care specifically for each nosological form. The article discusses the role of interhemispheric asymmetry in the pathogenesis of cerebrovascular diseases and effectiveness of the method of transcranial electrostimulation with feedback in the form of electroencephalography using the apparatus TATOS in the rehabilitation of patients with cerebrovascular pathology, including early recovery period of ischemic stroke Purpose: to identify clinical and neurophysiological features in patients with cerebrovascular pathology during transcranial electrotherapy with feedback. Material and methods. Total 105 patients with vascular pathology of the brain were studied, including 35 patients after ischemic stroke in the early recovery period with mild or moderate neurological symptoms, 70 patients with chronic cerebrovascular insufficiency. The average age is 56 3.6 years old. A comprehensive clinical, neurophysiological, and neuroimaging study was conducted. The course of non-invasive neuromodulation was performed against the background of medical treatment in accordance with the medical standards with the use of a pulse generator TETOS with feedback in the form of electroencephalography. Results. The study of the parameters of neurodynamic interhemispheric asymmetry showed that in patients who underwent onmc in the left middle cerebral artery basin, the localization of the ischemic lesion in the right middle cerebral artery basin was observed in the form of an increase in the interhemispheric coherence of the main electro-encephalographical rhythms with a predominance of slow-wave activity. After a course of non-invasive neuromodulation, the majority of patients in the main group noted an improvement in their well-being: headaches, dizziness, irritability, anxiety and anxiety, tension, significantly improved emotional state, and sleep normalized. The study of parameters of dynamic interhemispheric asymmetry has shown that when conducting transcranial electrotherapy with feedback in patients who have undergone stroke, depending on the localization, its decrease is noted, as well as normalization of the distribution of alpha rhythm in zones, depending on the localization of the focus. Conclusions. The overall assessment of the effect of treatment in the whole group revealed a clear prevalence of positive results when using TАTOS-therapy.

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Alexander Akhmedov ◽  
Remo D Spescha ◽  
Francesco Paneni ◽  
Giovani G Camici ◽  
Thomas F Luescher

Background— Stroke is one of the most common causes of death and long term disability worldwide primarily affecting the elderly population. Lectin-like oxidized LDL receptor 1 (LOX-1) is the receptor for oxidized LDL identified in endothelial cells. Binding of OxLDL to LOX-1 induces several cellular events in endothelial cells, such as activation of transcription factor NF-kB, upregulation of MCP-1, and reduction in intracellular NO. Accumulating evidence suggests that LOX-1 is involved in endothelial dysfunction, inflammation, atherogenesis, myocardial infarction, and intimal thickening after balloon catheter injury. Interestingly, a recent study demonstrated that acetylsalicylic acid (aspirin), which could prevent ischemic stroke, inhibited Ox-LDL-mediated LOX-1 expression in human coronary endothelial cells. The expression of LOX-1 was increased at a transient ischemic core site in the rat middle cerebral artery occlusion model. These data suggest that LOX-1 expression induces atherosclerosis in the brain and is the precipitating cause of ischemic stroke. Therefore, the goal of the present study was to investigate the role of endothelial LOX-1 in stroke using experimental mouse model. Methods and Results— 12-week-old male LOX-1TG generated recently in our group and wild-type (WT) mice were applied for a transient middle cerebral artery occlusion (MCAO) model to induce ischemia/reperfusion (I/R) brain injury. LOX-1TG mice developed 24h post-MCAO significantly larger infarcts in the brain compared to WT (81.51±8.84 vs. 46.41±10.13, n=7, p < 0.05) as assessed morphologically using Triphenyltetrazolium chloride (TTC) staining. Moreover, LOX-1TG showed higher neurological deficit in RotaRod (35.57±8.92 vs. 66.14±10.63, n=7, p < 0.05) and Bederson tests (2.22±0.14 vs. 1.25±0.30, n=9-12, p < 0.05) - two experimental physiological tests for neurological function. Conclusions— Thus, our data suggest that LOX-1 plays a critical role in the ischemic stroke when expressed at unphysiological levels. Such LOX-1 -associated phenotype could be due to the endothelial dysfunction. Therefore, LOX-1 may represent novel therapeutic targets for preventing ischemic stroke.


2021 ◽  
Vol 63 (1) ◽  
pp. 22-25
Author(s):  
Denys N. Khramtsov ◽  
Olexandr N. Stoyanov ◽  
Tetiana N. Muratova ◽  
Olexandr R. Pulyk

Aim: The aim of the study was to evaluate the clinical outcome in the use of neuroprotective agents in the acute period of ischemic stroke. Material and Methods: The study was performed on the basis of the stroke of the Center for Reconstructive and Rehabilitation Medicine (University Clinic) of the Odessa National Medical University. A retrospective analysis of clinical outcomes of 115 patients with acute stroke was conducted. Results: An average NIHSS score at discharge was 4.1±0.1 points when treated with no refinery, then it reached 3.6±0.1 points when using peptidergic drugs, and 3.4±0.1 when using D-fdf. 3.1±0.1 points. When using D-FDF, the MMSE score was 3.5±0.1 points, whereas when using cholinergic agents, this index did not exceed 26.9±1.5 points, and when using peptidergic agents - 26.8±1.4 points. Conclusion: The use of neuroprotective agents positively affects the effectiveness of neuro-rehabilitation in patients with acute stroke. The best results in three months after the hospitalization were obtained for peptidergic agents and D-fructose-1,6-diphosphate.


2020 ◽  
Vol 40 (12) ◽  
pp. 2837-2844 ◽  
Author(s):  
Jan Wenzel ◽  
Dimitrios Spyropoulos ◽  
Julian Christopher Assmann ◽  
Mahtab Ahmad Khan ◽  
Ines Stölting ◽  
...  

Objective: THBD (thrombomodulin) is part of the anticoagulant protein C-system that acts at the endothelium and is involved in anti-inflammatory and barrier-stabilizing processes. A recombinant soluble form of THBD was shown to have protective effects in different organs, but how the endogenous THBD is regulated during ischemia, particularly in the brain is not known to date. The aim of this study was to investigate the role of THBD, especially in brain endothelial cells, during ischemic stroke. Approach and Results: To induce ischemic brain damage, we occluded the middle cerebral artery of mice. We found an increased endothelial expression of Thbd in the peri-infarct area, whereas in the core of the ischemic tissue Thbd expression was decreased compared with the contralateral side. We generated a novel Cre/loxP-based mouse line that allows for the inducible deletion of Thbd specifically in brain endothelial cells, which worsened stroke outcome 48 hours after middle cerebral artery occlusion. Unexpectedly, we found no signs of increased coagulation, thrombosis, or inflammation in the brain but decreased vessel diameters and impaired angiogenesis in the peri-infarct area that led to a reduced overall vessel length 1 week after stroke induction. Conclusions: Endogenous THBD acts as a protective factor in the brain during ischemic stroke and enhances vessel diameter and proliferation. These previously unknown properties of THBD could offer new opportunities to affect vessel function after ischemia and thereby improve stroke outcome.


2019 ◽  
Vol 50 (2) ◽  
pp. 149-155
Author(s):  
I. A. Belayeva ◽  
M. Yu. Martynov ◽  
Ya. G. Pehova ◽  
A. A. Vershinin ◽  
A. P. Rachin ◽  
...  

2021 ◽  
Vol 121 (11) ◽  
pp. 26
Author(s):  
S.V. Kotov ◽  
V.A. Borisova ◽  
E.V. Slyunkova ◽  
E.V. Isakova ◽  
A.V. Kiselev ◽  
...  

2021 ◽  
Vol 17 (5) ◽  
pp. 23-34
Author(s):  
A. M. Golubev ◽  
A. V. Grechko ◽  
V. E. Zakharchenko ◽  
M. M. Kanarsky ◽  
M. V. Petrova ◽  
...  

According to epidemiological studies, the leading cause of morbidity, disability and mortality are cerebrovascular diseases, in particular ischemic and hemorrhagic strokes. In recent years considerable attention has been given to the study of molecular markers of ischemic and hemorrhagic strokes. These studies are relevant because brain-specific protein biomarkers of neurons and glial cells can provide valuable and timely diagnostic information necessary for clinical decision-making.The aim of the study was to reveal the differences in the serum level of molecular markers in acute, subacute and early recovery periods of ischemic and hemorrhagic strokes.Material and methods. The study included 59 patients. Twenty patients were diagnosed with hemorrhagic stroke and 39 had ischemic stroke. The control group included 20 volunteers. Serum levels of molecular CNS markers were determined in acute, subacute, and early recovery stages of stroke. The serum levels of CNS molecular markers of patients with ischemic and hemorrhagic stroke was measured quantitatively by enzyme immunoassay. Statistical analysis was performed by nonparametric Mann-Whitney method.Results. The level of brain-derived neurotrophic factor (BDNF) in the control volunteers was 574.5 [455.5; 615] pg/ml. Significant differences were found for acute and subacute periods of hemorrhagic stroke: it was 674 [560; 749] pg/ml (P=0.003) and 664 [616; 762] pg/ml (P=0.0001).The level of neuron-specific enolase was significantly increased in all periods of the study: it was 4.15 [3.53; 4.8] ng/ml in the control group, 5.4 [4.4; 6.4] ng/ml in acute period of ischemic stroke (P<0.001), 5.4 [4.4; 6.4] ng/ml in early recovery period of ischemic stroke (P=0.001), 5.1 [4.6; 6.4] ng/ml in acute period of hemorrhagic stroke (P=0.014), 664 [616; 762] ng/ml in subacute period of hemorrhagic stroke (P=0.003).In the control group, the serum S-100 protein level was 4.5 [3.8; 5.4] ng/ml. In the acute and early recovery periods of ischemic stroke, S-100 protein level has significantly fallen down to 4.1 [3.4; 4.6] ng/ml (P<0.031) and 3.9 [3.4; 6] ng/ml (P=0.014), respectively. Glial-cell derived neurotrophic factor level was 1.98 [1.64; 2.1] ng/ml in the controls and increased up to 2.4 [2.2; 5] ng/ml (P=0.002) in the acute period and 2.4 [2.3; 2.6] ng/ml (P<0.001) in the subacute period of hemorrhagic stroke.The vascular endothelial growth factor receptor-1 (VEGFR-1) was significantly lower in the subacute period of hemorrhagic stroke: 485 [211; 945] pg/ml in the subacute period vs 903.5 [626; 1115] pg/ml in the controls (P=0.001).Conclusion. We found differences in the serum level of molecular markers in patients with ischemic and hemorrhagic strokes. In the acute period, early recovery period of ischemic stroke, and subacute period of hemorrhagic stroke, there was an increase in the serum level of neuron-specific enolase. The level of brain-derived neurotrophic factor increased significantly in the acute and subacute periods of hemorrhagic stroke. In the acute and early recovery periods of ischemic stroke, the level of S-100 protein decreased. The level of glial cell-derived neurotrophic factor increased in the acute and subacute periods of hemorrhagic stroke. In the subacute period of hemorrhagic stroke, the level of endothelial growth factor receptor-1 significantly decreased. Moreover, there was significant difference between values of this parameter in the subacute period of hemorrhagic stroke and in the early recovery period of ischemic stroke.


2021 ◽  
Vol 26 (4) ◽  
pp. 31-38
Author(s):  
E. I. Nikishina ◽  
A. E. Danilova ◽  
V. B. Nikishina ◽  
I. V. Zapesotskaya ◽  
T. V. Nedurueva ◽  
...  

The article presents the results of the research of the features of the anticipation and prognostic function in patients with ischemic stroke of frontal localization in the early recovery period.Material and methods. The total sample group was represented by 60 patients who had suffered an ischemic stroke of frontal or parietal localization. The average age of the research subjects was 53.00 ± 5.44 years. The study was conducted with the use of functional neuropsychological tests (by A.R. Luria, L.S. Tsvetkova), methods of predictive function research (time estimation test, spatial anticipation test, Maze test, London Tower test, “incomplete images” test), as well as statistical methods of quantitative and qualitative data processing.Results. In patients with prefrontal localization of ischemic stroke a specific impairment of prognostic function and a non-specific decrease in anticipation were revealed. It is due to disorders of mental activity purposefulness and preliminary orientation in the conditions of the task. When the lesion was localized in the premotor areas, a less significant decrease in the rate and accuracy of the prognostic function due to the inertia of the mental processes was revealed. In the localization of ischemic stroke in the associative parietal cortex, a specific decrease in the rate and accuracy of sensorimotor, perceptual, and temporal anticipation was revealed, as well as a non-specific decrease in the rate of planning, while maintaining its accuracy of implementation.Conclusion. In terms of practical significance, taking into account the features of prognostic function that have arisen in a particular form of brain damage can serve as a basis for restoring other gnostic or motor impaired functions, increasing the effectiveness of correctional and rehabilitation measures.


2016 ◽  
Vol 116 (3. Vyp. 2) ◽  
pp. 48 ◽  
Author(s):  
O. A. Mudrova ◽  
N. B. Schekolova ◽  
F. A. Borikov

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