FEATURES OF CEREBRAL CIRCULATORY DYNAMICS AND CEREBRAL BIOELECTRIC ACTIVITY IN CHILDREN WITH CRANIOCEREBRAL INJURY

2020 ◽  
pp. 55-59
Author(s):  
Viktoriia Mykolaivna Petrenko

In order to study the state of cerebral hemodynamics and to investigate the electroencephalographic characteristics in children with closed traumatic brain injury, 114 patients were examined. The children were examined in 6.1±0.8 months after a traumatic brain injury. To determine cerebral hemodynamics, transcranial dopplerography was performed, the functional state of brain was evaluated according to electroencephalography. In the course of the study, it was noted that a disordered cerebral hemodynamics in children with moderate and severe brain contusion and its foci presence was accompanied by a rise in a linear velocity of blood flow, while its decrease was found at the same contusion, but that was severe and with the presence of subdural, subarachnoid and epidural hemorrhage. Signs of diffuse changes in bioelectrical activity of the brain were represented by a significant increase in an amplitude of the alpha rhythm in children with closed traumatic brain injury of moderate and serious severities compared to mild one. Key words: children, craniocerebral injury, electroencephalography, transcranial Doppler sonography, paroxysmal activity.

1982 ◽  
Vol 63 (6) ◽  
pp. 9-11
Author(s):  
A. L. Kirillov

Examined 87 patients with craniostenosis at the age from 3 to 14 years, who had suffered a moderate craniocerebral injury. It was found that in the stage of compensation, a relatively mild traumatic brain injury leads to mild brain contusion. Treatment of patients in this category should be conservative, but longer than in patients without concomitant craniostenosis. In the decompensated stage of craniostenosis, a similar injury causes the development of moderate brain contusion. With severe cerebral edema, flap craniotomy is indicated, since conventional dehydration therapy is ineffective.


Neurosurgery ◽  
2011 ◽  
Vol 68 (3) ◽  
pp. 588-600 ◽  
Author(s):  
Charles S. Cox ◽  
James E. Baumgartner ◽  
Matthew T. Harting ◽  
Laura L. Worth ◽  
Peter A. Walker ◽  
...  

Abstract BACKGROUND: Severe traumatic brain injury (TBI) in children is associated with substantial long-term morbidity and mortality. Currently, there are no successful neuroprotective/neuroreparative treatments for TBI. Numerous preclinical studies suggest that bone marrow-derived mononuclear cells (BMMNCs), their derivative cells (marrow stromal cells), or similar cells (umbilical cord blood cells) offer neuroprotection. OBJECTIVE: To determine whether autologous BMMNCs are a safe treatment for severe TBI in children. METHODS: Ten children aged 5 to 14 years with a postresuscitation Glasgow Coma Scale of 5 to 8 were treated with 6 × 106 autologous BMMNCs/kg body weight delivered intravenously within 48 hours after TBI. To determine the safety of the procedure, systemic and cerebral hemodynamics were monitored during bone marrow harvest; infusion-related toxicity was determined by pediatric logistic organ dysfunction (PELOD) scores, hepatic enzymes, Murray lung injury scores, and renal function. Conventional magnetic resonance imaging (cMRI) data were obtained at 1 and 6 months postinjury, as were neuropsychological and functional outcome measures. RESULTS: All patients survived. There were no episodes of harvest-related depression of systemic or cerebral hemodynamics. There was no detectable infusion-related toxicity as determined by PELOD score, hepatic enzymes, Murray lung injury scores, or renal function. cMRI imaging comparing gray matter, white matter, and CSF volumes showed no reduction from 1 to 6 months postinjury. Dichotomized Glasgow Outcome Score at 6 months showed 70% with good outcomes and 30% with moderate to severe disability. CONCLUSION: Bone marrow harvest and intravenous mononuclear cell infusion as treatment for severe TBI in children is logistically feasible and safe.


2009 ◽  
Vol 8 (1) ◽  
pp. 61-63
Author(s):  
D. V. Kolmakov

In this work, we have analyzed 2 774 case records of children after traumatic brain injury for the period of 2003 to 2007 (based on materials of the Tomsk Municipal Children’s Hospital No. 4). The age structure and causes of a traumatic brain injury have been analyzed. Most often complaints of children coming to the hospital are revealed, as well as typical changes in the cerebral hemodynamics (from the data of по данным rheoencephalography) and some parameters characterizing the neurological status of patients immediately after the injury and six months later. Based on the analysis of case records and health status questionnaires of children having traumatic brain injury up to six months later, it is shown that parents of patients in some cases do not adhere doctor’s recommendations after leaving the hospital. The therapy of traumatic brain injury in children requires successive treatment in hospital and at home and development of simple and acceptable rehabilitation schemes for children.


Author(s):  
M.S. Shuvalova ◽  
A.S. Shanazarov ◽  
Yu.Kh.-M. Shidakov

Mountains occupy about 24 % of the land surface. There are significant natural resources here, the development of which is associated with an increased traumatic risk. Craniocerebral injuries in the mountains are very frequent, and microvascular dysfunction, as under ordinary conditions, is a key element in the chain of events in the central nervous system. However, there are very few data on vascular plexuses and brain microcirculation in craniocerebral injury that occurs in the mountains. The aim of the study is to reveal the patterns in remodeling of vascular plexuse and main elements of brain microcirculation in craniocerebral injury that occurs in the mountains. Materials and Methods. The study enrolled 46 white outbred male laboratory rats (210–270 g) with simulated low-mountain (760 m above sea level, Bishkek) and high- mountains (Too Ashuu mountain pass, 3200 m above sea level) traumatic brain injury. The authors used the weight-drop method (Y. Tang technique) to reproduce the traumatic brain injury. After reproduction of the trauma in high altitudes, the animals were transported to low altitudes and on the 3rd day the rats were sacrificed with chloroform overdose. The authors studied microcirculation using a microscopic method with black ink intravascular injection. Olympus Bx40 microscope (Japan) was used for this purpose. At the same time, serial microphotography with simultaneous recording of the results was carried out using a digital camera connected to a computer. The morphometry of the vascular plexuse brain components was carried out with Top View application used for measuring microscopic objects. SPSS 16.0 software was used to process statistical data. Results. Craniocerebral injury that occurs in high mountains causes the narrowing of the capillary lumen by 52 % (p<0.001). In comparison with low mountains, the capillary lumen in high mountains decreases by 42 % (p<0.001). Venous plethora is observed. In vascular plexuses in the highlands, remodeling of the cellular component is recorded: ependymocyte volume increases by 23 % (p<0.05), nucleus volume – by 30 % (p<0.001), and cytoplasm volume – by 22 % (p<0.05). Conclusion. Craniocerebral injury leads to the development of cytotoxic edema in the vascular plexus stroma and to remodeling of brain microcirculation, which is the pathogenetic basis for hypertension and increased intracranial pressure. In the highlands, these phenomena are more pronounced and are accompanied by blood flow centralization. Keywords: microcirculation, vascular plexuses, brain, craniocerebral injury, highlands. Горы занимают около 24 % территории суши. Здесь располагаются значительные природные ресурсы, освоение которых сопряжено с повышенным риском травматизма. Черепно-мозговая травма на горных высотах – частое явление, а микрососудистая дисфункция, как и в обычных условиях обитания человека, является ключевым звеном в цепи событий, развертывающихся в центральной нервной системе. Однако данных о состоянии сосудистых сплетений и микроциркуляции головного мозга при черепно-мозговой травме, возникшей в высокогорье, крайне мало. Цель исследования – выявить закономерности ремоделирования сосудистых сплетений и основных звеньев микроциркуляции головного мозга при черепно-мозговой травме, возникшей в условиях высокогорья. Материалы и методы. Объектом исследования послужили 46 белых беспородных лабораторных крыс-самцов весом 210–270 г, которым моделировалась черепно-мозговая травма в условиях низкогорья (высота 760 м над уровнем моря, г. Бишкек) и высокогорья (перевал Туя-Ашу, 3200 м над уровнем моря). Для воспроизведения черепно-мозговой травмы использовалась ударная модель weight drop method по Y. Tang. После воспроизведения травмы в условиях высокогорья животных транспортировали в условия низкогорья и на 3-и сут выводили из эксперимента путем передозировки хлороформа. Микроциркуляция изучалась микроскопическим методом с применением внутрисосудистого инъецирования раствором черной туши. Препараты изучались под микроскопом Olympus Bx40 (Япония). Параллельно проводилось серийное микрофотографирование с помощью цифрового фотоаппарата, подключенного к компьютеру, с одновременным протоколированием результатов. Морфометрия компонентов сосудистых сплетений головного мозга осуществлялась с помощью приложения для измерения микроскопических объектов Top View. Статистическая обработка данных проводилась в программе SPSS 16.0. Результаты. Черепно-мозговая травма, возникшая в условиях высокогорья, приводит к сужению просвета капилляров на 52 % (p<0,001), при этом в сравнении с низкогорьем просвет капилляров в высокогорье уменьшается на 42 % (p<0,001). Отмечаются явления венозного полнокровия. Со стороны сосудистых сплетений в высокогорье регистрируется ремоделирование клеточного компонента: объем эпендимоцитов возрастает на 23 % (p<0,05), объем ядра – на 30 % (p<0,001), объем цитоплазмы – на 22 % (p<0,05). Выводы. Черепно-мозговая травма привела к развитию цитотоксического отека стромы сосудистого сплетения и ремоделированию системы микроциркуляции головного мозга, что является патогенетической основой гипертензии и повышения внутричерепного давления. В высокогорье эти явления выражены в большей степени и сопровождаются признаками централизации кровообращения. Ключевые слова: микроциркуляция, сосудистые сплетения, головной мозг, черепно-мозговая травма, высокогорье.


2020 ◽  
pp. 0271678X2096259
Author(s):  
Amreen Mughal ◽  
Adrian M Sackheim ◽  
Maria Sancho ◽  
Thomas A Longden ◽  
Sheila Russell ◽  
...  

Traumatic brain injury (TBI) acutely impairs dynamic regulation of local cerebral blood flow, but long-term (>72 h) effects on functional hyperemia are unknown. Functional hyperemia depends on capillary endothelial cell inward rectifier potassium channels (Kir2.1) responding to potassium (K+) released during neuronal activity to produce a regenerative, hyperpolarizing electrical signal that propagates from capillaries to dilate upstream penetrating arterioles. We hypothesized that TBI causes widespread disruption of electrical signaling from capillaries-to-arterioles through impairment of Kir2.1 channel function. We randomized mice to TBI or control groups and allowed them to recover for 4 to 7 days post-injury. We measured in vivo cerebral hemodynamics and arteriolar responses to local stimulation of capillaries with 10 mM K+ using multiphoton laser scanning microscopy through a cranial window under urethane and α-chloralose anesthesia. Capillary angio-architecture was not significantly affected following injury. However, K+-induced hyperemia was significantly impaired. Electrophysiology recordings in freshly isolated capillary endothelial cells revealed diminished Ba2+-sensitive Kir2.1 currents, consistent with a reduction in channel function. In pressurized cerebral arteries isolated from TBI mice, K+ failed to elicit the vasodilation seen in controls. We conclude that disruption of endothelial Kir2.1 channel function impairs capillary-to-arteriole electrical signaling, contributing to altered cerebral hemodynamics after TBI.


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