Extracellular Mitochondria in Traumatic Brain Injury Induced Coagulopathy

2019 ◽  
Vol 46 (02) ◽  
pp. 167-175
Author(s):  
Zilong Zhao ◽  
Yuan Zhou ◽  
Min Li ◽  
Jianning Zhang ◽  
Jing-Fei Dong
Keyword(s):  
Traumatic Brain Injury ◽  
Endothelial Cells ◽  
Brain Injury ◽  
Tissue Injury ◽  
The Body ◽  
Secondary Tissue ◽  
Dilutional Coagulopathy ◽  
Poor Outcomes ◽  
Traumatic Impact

AbstractTraumatic brain injury (TBI) induced coagulopathy remains a significant clinical challenge, with unmet needs for standardizing diagnosis and optimizing treatments. TBI-induced coagulopathy is closely associated with poor outcomes in affected patients. Recent studies have demonstrated that TBI induces coagulopathy, which is mechanistically distinct from the deficient and dilutional coagulopathy found in patients with injuries to the body/limbs and hemorrhagic shock. Multiple causal and disseminating factors have been identified to cause TBI-induced coagulopathy. Among these are extracellular mitochondria (exMTs) released from injured cerebral cells, endothelial cells, and platelets. These circulating exMTs not only express potent procoagulant activity but also promote inflammation, and could remain metabolically active to become a major source of oxidative stress. They activate platelets and endothelial cells to propagate TBI-induced coagulopathy and secondary tissue injury after primary traumatic impact. In this review, we discuss recent advances in our understanding of the role of exMTs in the development of TBI-induced coagulopathy.

scholarly journals Clinical and epidemiological analysis of severe traumatic brain injury: the role of nutritional support to the injured with a prolonged state of impaired consciousness

2020 ◽  
pp. 32-43
Author(s):  
M. V. Nikiforov ◽  
A. A. Korolev
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Nutritional Support ◽  
The Body ◽  
Medical Rehabilitation ◽  
Impaired Consciousness ◽  
Epidemiological Analysis ◽  
The Brain

Relevance. Patients with prolonged impaired consciousness due to traumatic brain injury are the most difficult category of patients in inpatient medical rehabilitation units. Despite the experience gained in managing this complex category of patients, the problem of nutrition status and trophological insufficiency, as well as practical issues regarding the organization of optimal nutrition at this stage of medical rehabilitation remain unresolved.Intention. To study the role of nutritional support for patients with long-term impaired consciousness on the basis of a clinical and epidemiological analysis of severe traumatic brain injury.Methodology. The data of an epidemiological analysis of traumatic brain injuries and features of ongoing nutritional support in patients with long-term impaired consciousness are presented, based on a study of domestic and foreign publications from 2005 to 2019.Results and Discussion. Timely and adequate nutritional support optimizes the structural-functional and metabolic systems of the body, adaptive reserves interfere with rapidly progressive depletion and chronic catabolic processes, contribute to positive changes in the functional state of the brain, reduce infectious complications, and increase the effectiveness of rehabilitation measures and the rate of recovery of consciousness.Conclusion. The analysis revealed the ambiguity of the interpreted data on clinical recommendations and approaches to the use of nutritional support in patients with long-term impaired consciousness due to traumatic brain injury. Considering the fact that in most cases such patients need continuous long-term comprehensive rehabilitation measures, accompanied by significant energy costs of the body, an essential component of the rehabilitation process, in our opinion, is the inclusion of adequate nutritional support that prevents fast-progressing exhaustion and chronic catabolic processes. In this regard, such an urgent task is to optimize the algorithms of nutritional support in patients with long-term impaired consciousness after a traumatic brain injury, the solution of which will improve the functional state of the brain and, therefore, the rehabilitation prognosis and quality of their life.

scholarly journals Adenosine A3 receptor as a novel therapeutic target to reduce secondary events and improve neurocognitive functions following traumatic brain injury

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Susan A. Farr ◽  
Salvatore Cuzzocrea ◽  
Emanuela Esposito ◽  
Michela Campolo ◽  
Michael L. Niehoff ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Tissue Injury ◽  
Pathological Condition ◽  
Brain Infarction ◽  
Inflammasome Activation ◽  
Secondary Brain Injury ◽  
Male Mice ◽  
Neuroprotective Effects ◽  
Secondary Tissue

Abstract Background Traumatic brain injury (TBI) is a common pathological condition that presently lacks a specific pharmacological treatment. Adenosine levels rise following TBI, which is thought to be neuroprotective against secondary brain injury. Evidence from stroke and inflammatory disease models suggests that adenosine signaling through the G protein-coupled A3 adenosine receptor (A3AR) can provide antiinflammatory and neuroprotective effects. However, the role of A3AR in TBI has not been investigated. Methods Using the selective A3AR agonist, MRS5980, we evaluated the effects of A3AR activation on the pathological outcomes and cognitive function in CD1 male mouse models of TBI. Results When measured 24 h after controlled cortical impact (CCI) TBI, male mice treated with intraperitoneal injections of MRS5980 (1 mg/kg) had reduced secondary tissue injury and brain infarction than vehicle-treated mice with TBI. These effects were associated with attenuated neuroinflammation marked by reduced activation of nuclear factor of kappa light polypeptide gene enhancer in B cells (NFκB) and MAPK (p38 and extracellular signal-regulated kinase (ERK)) pathways and downstream NOD-like receptor pyrin domain-containing 3 inflammasome activation. MRS5980 also attenuated TBI-induced CD4+ and CD8+ T cell influx. Moreover, when measured 4–5 weeks after closed head weight-drop TBI, male mice treated with MRS5980 (1 mg/kg) performed significantly better in novel object-placement retention tests (NOPRT) and T maze trials than untreated mice with TBI without altered locomotor activity or increased anxiety. Conclusion Our results provide support for the beneficial effects of small molecule A3AR agonists to mitigate secondary tissue injury and cognitive impairment following TBI.

Role of innate inflammation in traumatic brain injury

2021 ◽  
Author(s):  
Sandrine Bourgeois-Tardif ◽  
Louis De Beaumont ◽  
José Carlos Rivera ◽  
Sylvain Chemtob ◽  
Alexander G Weil
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury

scholarly journals P88 Paroxysmal sympathetic storm and the role of beta-blockers in traumatic brain injury: a scoping review protocol

BJS Open ◽  
2021 ◽  
Vol 5 (Supplement_1) ◽  
Author(s):  
Stéphane Nguembu ◽  
Marco Meloni ◽  
Geneviève Endalle ◽  
Hugues Dokponou ◽  
Olaoluwa Ezekiel Dada ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Length Of Stay ◽  
Glasgow Coma Scale ◽  
Scoping Review ◽  
Beta Blockers ◽  
Clinical Signs ◽  
Sympathetic Hyperactivity ◽  
Paroxysmal Sympathetic Hyperactivity

Abstract Introduction Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Method We will search MEDLINE, Web of Science, EMBASE, Cochrane, and Google Scholar. The search terms used will cover the following terms: “paroxysmal sympathetic hyperactivity”, “traumatic brain injury” and “beta-blockers.”: No language or geographical restrictions will be applied. Two independent co-authors will screen the titles and abstracts of each article following predefined inclusion and exclusion criteria. If there is a conflict the two reviewers will find a consensus and if they cannot a third co-author will decide. Using a pre-designed and pre-piloted data extraction form, data from each included citation will be collected (authors identification, study type, TBI severity, type of beta-blockers used, dosage of the drug, clinical signs of PSH, Glasgow Coma Scale, Glasgow Outcome Scale, mortality, morbidity and length of stay). Simple descriptive data analyses will be performed and the results will be presented both in a narrative and tabular form. Results The effectiveness of beta-blockers in post-TBI PHS will be evaluated through clinical signs of PHS(increased heart rate, respiratory rate, temperature, blood pressure, and sweating), Glasgow Coma Scale, and Glasgow Outcome Scale. mortality, morbidity and length of stay. Conclusion At the end of this scoping review we will design a systematic review with metaanalysis if there are a reasonable number of studies otherwise we will design a randomized controlled trial.

Polydatin alleviates traumatic brain injury: Role of inhibiting ferroptosis

2021 ◽  
Vol 556 ◽  
pp. 149-155
Author(s):  
Lu Huang ◽  
Shulei He ◽  
Qing Cai ◽  
Fei Li ◽  
Siwei Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury

scholarly journals Creatine Supplementation and Brain Health

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 586 ◽  
Author(s):  
Hamilton Roschel ◽  
Bruno Gualano ◽  
Sergej M. Ostojic ◽  
Eric S. Rawson
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Function ◽  
Cognitive Processing ◽  
Brain Function ◽  
Creatine Supplementation ◽  
Short Review ◽  
Future Research ◽  
Brain Health

There is a robust and compelling body of evidence supporting the ergogenic and therapeutic role of creatine supplementation in muscle. Beyond these well-described effects and mechanisms, there is literature to suggest that creatine may also be beneficial to brain health (e.g., cognitive processing, brain function, and recovery from trauma). This is a growing field of research, and the purpose of this short review is to provide an update on the effects of creatine supplementation on brain health in humans. There is a potential for creatine supplementation to improve cognitive processing, especially in conditions characterized by brain creatine deficits, which could be induced by acute stressors (e.g., exercise, sleep deprivation) or chronic, pathologic conditions (e.g., creatine synthesis enzyme deficiencies, mild traumatic brain injury, aging, Alzheimer’s disease, depression). Despite this, the optimal creatine protocol able to increase brain creatine levels is still to be determined. Similarly, supplementation studies concomitantly assessing brain creatine and cognitive function are needed. Collectively, data available are promising and future research in the area is warranted.

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