scholarly journals ROLE OF THE CELLULAR IMMUNITY IN THE PATHOGENESIS OF BRAIN CONTUSION

2021 ◽  
Vol 23 (4) ◽  
pp. 825-830
Author(s):  
A. O. Norka ◽  
S. V. Vorobyev ◽  
R. N. Kuznetsova ◽  
M. K. Serebriakova ◽  
I. V. Kudryavtsev ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Immune System ◽  
Brain Injury ◽  
Nervous Tissue ◽  
Immune Status ◽  
Early Period ◽  
Current Evidence ◽  
Control Group ◽  
Brain Contusion ◽  
The Brain

Traumatic brain injury (TBI) is one of the most common pathologies of the central nervous system in the world, and the use of structural neuroimaging methods – computed tomography (CT) and magnetic resonance imaging (MRI) – often doesn’t allow assessment of the severity of the brain injury that has occurred. This situation predetermines the need to search for new methods of differential diagnosis of the severity of TBI and predicting the risk of consequences.One of these promising areas is the study of the immune status, since traumatic brain injury is characterized by a high rate of complications.One of these promising areas is the study of the immune status in patients with TBI in the acute period. It is now known that in response to brain damage, a response from the immune system is triggered.The reactions from the immune system, which develop after brain injury and directed against its own antigens, in the early period of the disease are related to damage to the nervous tissue. However, according to the latest available data, they are subsequently able to stimulate the processes of repair and regeneration in the brain tissue. In the course of damage to the nervous tissue, in response to endogenous molecules formed during the destruction of cells and the extracellular matrix, the cells of the immune system are activated.Current evidence indicates that T-cells play a role in both the formation of secondary damage and repair mechanisms. They are able to protect neurons through the production of neurotrophic factors such as brain neurotrophic factor (BDNF), which stimulates the growth of neurons, the formation of synapses.Using multicolor cytometric analysis within the framework of this work, a study was carried out to determine the number of the main subpopulations of CD3+CD4+-lymphocytes. The relative number of Th17 (CXCR5- CXCR3- CCR6+CCR4- ) and Th17/Th22 (CXCR5- CXCR3- CCR6+CCR4+), Th1/Th17 (CXCR5- CXCR3+CCR6+CCR4- ) among total CD45RA-negative CD3+CD4+-cells population is significantly increased in comparison with the values in the control group, in turn, the Th1(CXCR5- CXCR3+CCR6- CCR4- ) subpopulations among total CD45RA-negative CD3+CD4+-cells are significantly decreased with the values in the control group. The results obtained so far make it possible to consider immune responses among the key links in the pathogenesis of brain contusion TBI. And, perhaps, a comprehensive immunological examination of the victims in the first day after the injury will determine the parameters that will help predict the nature of possible complications in patients with brain contusion. 

scholarly journals NEURODESTRUCTION OF HYPOTHALAMIC NUCLEI IN BRAIN INJURY. EFFECT OF CARBACETAM

2018 ◽  
Vol 13 (3-4) ◽  
pp. 3-9
Author(s):  
S.V. Ziablitsev ◽  
T.I. Panova ◽  
O.O. Starodubska
Keyword(s):  
Brain Injury ◽  
Nervous Tissue ◽  
Free Fall ◽  
Benzodiazepine Receptor ◽  
Expression Level ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
The Brain ◽  
Supraoptic Nuclei

Relevance. A key role in the pathogenesis of brain injury (BI) is played by destructive changes in the neural tissue of the brain, which consist in damage to neurons and glial cells. To date, various drugs are being intensively developed and studied, which are considered in the perspective of correction and restoration of the functional state of the brain. These substances include the neuroprotector carbacetam, an modulator of the GABA-benzodiazepine receptor complex, a derivative of the alkaloid β-carboline. Objectie. To investigate the effect of carbacetam on neurodestruction processes in the paraventricular and supraoptic nuclei of the hypothalamus in experimental BI. Material and methods. The study was carried out on 20 white non-native male rats weighing 200±10 g. To simulate the BI, rats were subjected to one stroke along the cranial vault with a free-fall load according to the V.N. Yelskyy and S.V. Ziablitsev method (2008). The energy of impact was 0.52 J, the lethality for the first 5 days after injury was 84%. In the control group (n=10) 1 ml of saline was injected intraperitoneally once daily for 10 days after injury. Animals of the experimental group (n=10) received intraperitoneally injections of carbacetam at a dose of 5 mg/kg in 1 ml of saline according to the same scheme. After the experiment was over, the animals were decapitated with the removal of the brain, from which histological preparations were made with a microtome after appropriate histological treatment. Some sections were stained with hematoxylin and eosin, others were immunohistochemically reacted with antibodies against neuronmarkers proteins NSE, S-100 and GFAP. Results. Carbacetam influenced the decrease of degenerative processes in the nervous tissue of the paraventricular and supraoptic nuclei of the hypothalamus. Neurons of animals with BI that received carbacetam, were characterized by the restoration of normal morphological features in contrast to rats not receiving the drug. Immunohistochemical study of brain neuromarkers confirmed the restoration of the functions of neurons and astrocytes in the investigated parts of the rat's hypothalamus after the administration of carbacetam. There was a decrease in the expression level of glial markers GFAP and S-100, which illustrated the decrease in degenerative changes in the nervous tissue. While the expression level of the neuron marker NSE grew, this demonstrated the high metabolic activity of nerve cells. Changes in the expression of markers of neurons and glia indicated a restoration of normal neuronal activity under the action of carbacetam. Conclusion. Further investigation of the effects of carbacetam seems promising in terms of the restoration of neuronal function at BI.

scholarly journals Therapeutic Dilemmas regarding Anticoagulation: An Experience in a Patient with Nephrotic Syndrome, Pulmonary Embolism, and Traumatic Brain Injury

2016 ◽  
Vol 9 ◽  
pp. CCRep.S40607 ◽  
Author(s):  
Tetsu Akimoto ◽  
Tomoyuki Yamazaki ◽  
Eiji Kusano ◽  
Daisuke Nagata
Keyword(s):  
Traumatic Brain Injury ◽  
Pulmonary Embolism ◽  
Nephrotic Syndrome ◽  
Brain Injury ◽  
Bleeding Complications ◽  
Brain Contusion ◽  
Increased Risk ◽  
Substantial Risk ◽  
The Brain ◽  
Acute Pe

Patients with active bleeding complications who concomitantly develop overt pulmonary embolism (PE) present distinct therapeutic dilemmas, since they are perceived to be at substantial risk for the progression of the embolism in the absence of treatment and for aggravation of the hemorrhagic lesions if treated with anticoagulants. A 76-year-old patient with nephrotic syndrome, which is associated with an increased risk of thromboembolism, concurrently developed acute PE and intracranial bleeding because of traumatic brain injury. In this case, we prioritized the treatment for PE with the intravenous unfractionated heparin followed by warfarinization. Despite the transient hemorrhagic progression of the brain contusion after the institution of anticoagulation, our patient recovered favorably from the disease without any signs of neurological compromise. Several conundrums regarding anticoagulation that emerged in this case are also discussed.

scholarly journals Role of 5-HT in Cerebral Edema after Traumatic Brain Injury

2021 ◽  
Author(s):  
Priya Badyal ◽  
Jaspreet Kaur ◽  
Anurag Kuhad
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Nervous Tissue ◽  
Closed Head Injury ◽  
Cell Swelling ◽  
Volume Swelling ◽  
Cell Changes ◽  
Primary Injury ◽  
The Brain

The pathogenesis of edema after traumatic brain injury is complex including the destruction of micro-vessels and alterations in microcirculation around the primary injury and leakage of plasma constituents into the tissue, due to permeability changes of the vessel walls. Many functional molecules like histamine, serotonin, arachidonic acid, prostaglandins and thromboxane have been shown to induce blood–brain barrier (BBB) disruption or cell swelling. It is believed that released 5-HT binds to 5-HT2 receptors stimulating cAMP and prostaglandins in vessels that cause more vesicular transport in endothelial cells leading to serum component’s extravasation. The additional amount of serotonin into the tissue due to injury maintains the state of increased vascular permeability that ultimately causes edema. Serotonin is clearly involved in early cytotoxic edema after TBI. Reduction of serotonin in the nervous tissue reduces swelling and the milder cell changes in the brain or spinal cord of traumatized rats. Inhibition of serotonin synthesis before closed head injury (CHI) in rat models or administration of serotonin antiserum after injury attenuates BBB disruption and brain edema volume swelling, and brain pathology. Maintaining low serotonin levels immediately after injury may show neuroprotection and combat various secondary outcomes that occur after traumatic brain injury.

Lessons Learned From Coaching Postsecondary Students With Traumatic Brain Injury

2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy
Keyword(s):  
College Students ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Sense Of Self ◽  
Scientific Evidence ◽  
Sudden Onset ◽  
Lessons Learned ◽  
Speech Language Pathologists ◽  
The Brain ◽  
Exhaustive List

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.

Providing Care of Mild Traumatic Brain Injury by the Family Practice/Primary Care Optometrist

2018 ◽  
pp. 110-119
Keyword(s):  
Primary Care ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Family Practice ◽  
Advanced Training ◽  
Entry Level ◽  
The Family ◽  
Basic Understanding ◽  
The Brain

Primary Objectives: By extending the scope of knowledge of the primary care optometrist, the brain injury population will have expanded access to entry level neurooptometric care by optometric providers who have a basic understanding of their neurovisual problems, be able to provide some treatment and know when to refer to their colleagues who have advanced training in neuro-optometric rehabilitation.

scholarly journals Ulinastatin alleviates traumatic brain injury by reducing endothelin-1

2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Water Content ◽  
Brain Edema ◽  
Rat Model ◽  
Neurosurgical Procedures ◽  
Brain Water Content ◽  
The Brain ◽  
Brain Water

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.

scholarly journals Remotely delivered environmental enrichment intervention for traumatic brain injury: Study protocol for a randomised controlled trial

BMJ Open ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. e039767
Author(s):  
Zorry Belchev ◽  
Mary Ellene Boulos ◽  
Julia Rybkina ◽  
Kadeen Johns ◽  
Eliyas Jeffay ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Active Control ◽  
Environmental Enrichment ◽  
Spatial Navigation ◽  
Controlled Trial ◽  
Control Group ◽  
Hippocampal Atrophy ◽  
Active Control Group ◽  
Navigation Group

IntroductionIndividuals with moderate-severe traumatic brain injury (m-sTBI) experience progressive brain and behavioural declines in the chronic stages of injury. Longitudinal studies found that a majority of patients with m-sTBI exhibit significant hippocampal atrophy from 5 to 12 months post-injury, associated with decreased cognitive environmental enrichment (EE). Encouragingly, engaging in EE has been shown to lead to neural improvements, suggesting it is a promising avenue for offsetting hippocampal neurodegeneration in m-sTBI. Allocentric spatial navigation (ie, flexible, bird’s eye view approach), is a good candidate for EE in m-sTBI because it is associated with hippocampal activation and reduced ageing-related volume loss. Efficacy of EE requires intensive daily training, prohibitive within most current health delivery systems. The present protocol is a novel, remotely delivered and self-administered intervention designed to harness principles from EE and allocentric spatial navigation to offset hippocampal atrophy and potentially improve hippocampal functions such as navigation and memory for patients with m-sTBI.Methods and analysisEighty-four participants with chronic m-sTBI are being recruited from an urban rehabilitation hospital and randomised into a 16-week intervention (5 hours/week; total: 80 hours) of either targeted spatial navigation or an active control group. The spatial navigation group engages in structured exploration of different cities using Google Street View that includes daily navigation challenges. The active control group watches and answers subjective questions about educational videos. Following a brief orientation, participants remotely self-administer the intervention on their home computer. In addition to feasibility and compliance measures, clinical and experimental cognitive measures as well as MRI scan data are collected pre-intervention and post-intervention to determine behavioural and neural efficacy.Ethics and disseminationEthics approval has been obtained from ethics boards at the University Health Network and University of Toronto. Findings will be presented at academic conferences and submitted to peer-reviewed journals.Trial registration numberVersion 3, ClinicalTrials.gov Registry (NCT04331392).

scholarly journals Engineered glycomaterial implants orchestrate large-scale functional repair of brain tissue chronically after severe traumatic brain injury

2021 ◽  
Vol 7 (10) ◽  
pp. eabe0207
Author(s):  
Charles-Francois V. Latchoumane ◽  
Martha I. Betancur ◽  
Gregory A. Simchick ◽  
Min Kyoung Sun ◽  
Rameen Forghani ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Large Scale ◽  
Growth Factor Signaling ◽  
Neuronal Circuit ◽  
Reach To Grasp ◽  
Function Recovery ◽  
Cellular Repair ◽  
The Brain

Severe traumatic brain injury (sTBI) survivors experience permanent functional disabilities due to significant volume loss and the brain’s poor capacity to regenerate. Chondroitin sulfate glycosaminoglycans (CS-GAGs) are key regulators of growth factor signaling and neural stem cell homeostasis in the brain. However, the efficacy of engineered CS (eCS) matrices in mediating structural and functional recovery chronically after sTBI has not been investigated. We report that neurotrophic factor functionalized acellular eCS matrices implanted into the rat M1 region acutely after sTBI significantly enhanced cellular repair and gross motor function recovery when compared to controls 20 weeks after sTBI. Animals subjected to M2 region injuries followed by eCS matrix implantations demonstrated the significant recovery of “reach-to-grasp” function. This was attributed to enhanced volumetric vascularization, activity-regulated cytoskeleton (Arc) protein expression, and perilesional sensorimotor connectivity. These findings indicate that eCS matrices implanted acutely after sTBI can support complex cellular, vascular, and neuronal circuit repair chronically after sTBI.

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