Changes in Coagulation following Brain Injury

2020 ◽  
Vol 46 (02) ◽  
pp. 155-166
Author(s):  
Marc Maegele ◽  
John Aversa ◽  
Mathew K. Marsee ◽  
Ross McCauley ◽  
Swetha Hanuma Chitta ◽  
...  
Keyword(s):  
Brain Injury ◽  
Point Of Care ◽  
Activated Protein C ◽  
Brain Parenchyma ◽  
Health Concern ◽  
Cerebral Vasculature ◽  
Clinical Presentations ◽  
Initial Injury ◽  
The Brain ◽  
Supporting Structures

AbstractTraumatic brain injury (TBI) is a worldwide public health concern due to increasing mortality, affecting around 10 million patients per year. A wide variety of clinical presentations are a function of the magnitude of injury and the anatomical perturbation of the brain parenchyma, supporting structures, and cerebral vasculature, with subsequent alteration of the blood–brain barrier. These disturbances correspond with the evolution of intracerebral hemorrhage and clinical outcomes. The associated hemostatic alterations associated with TBI are caused by the disruption of the delicate balance between bleeding and thrombosis formation, which can exacerbate initial injury. TBI-associated coagulopathy is a function of a cross-talk between coagulation and inflammation, with varying influences on the immunomodulation and regulation of coagulation that occur on platelets and the endothelium of injured TBI patients. In addition to the severity of initial injury, the following factors modulate the hemocoagulative response to TBI: time from the onset of injury to treatment, age, gender, catecholamine secretion, platelet dysfunction, endotheliopathy, premorbid anticoagulation, fibrinolysis, tissue factor, and activated protein C contribution. All these entities are intertwined and influence the pathologic evolution of TBI. These factors have implications for therapeutic options such as the choice of blood components for transfusion and hemostatic agents such as tranexamic acid. Monitoring hemostatic changes of TBI patients requires an understanding of these interactions between immunology and coagulation, which can be discerned by point-of-care viscoelastic testing with specific limitations. This review considers the implications of these interrelated influences on the evaluation of coagulopathy in TBI.

scholarly journals Sport-related concussions

2014 ◽  
Vol 8 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Jéssica Natuline Ianof ◽  
Fabio Rios Freire ◽  
Vanessa Tomé Gonçalves Calado ◽  
Juliana Rhein Lacerda ◽  
Fernanda Coelho ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Behavioral Changes ◽  
American Football ◽  
Health Concern ◽  
Public Health Concern ◽  
Increased Risk ◽  
High Prevalence ◽  
Biomechanical Forces ◽  
The Brain

ABSTRACT Traumatic brain injury (TBI) is a major cause of lifelong disability and death worldwide. Sport-related traumatic brain injury is an important public health concern. The purpose of this review was to highlight the importance of sport-related concussions. Concussion refers to a transient alteration in consciousness induced by external biomechanical forces transmitted directly or indirectly to the brain. It is a common, although most likely underreported, condition. Contact sports such as American football, rugby, soccer, boxing, basketball and hockey are associated with a relatively high prevalence of concussion. Various factors may be associated with a greater risk of sport-related concussion, such as age, sex, sport played, level of sport played and equipment used. Physical complaints (headache, fatigue, dizziness), behavioral changes (depression, anxiety, irritability) and cognitive impairment are very common after a concussion. The risk of premature return to activities includes the prolongation of post-concussive symptoms and increased risk of concussion recurrence.

scholarly journals Neurogenesis and Oligodendrogenesis in a Mouse Model of Blast-Induced Traumatic Brain Injury

2020 ◽  
pp. 1-14
Author(s):  
Michal K. Stachowiak ◽  
D. Freedman ◽  
N. Nived ◽  
B. Decker ◽  
S. Narla ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Function ◽  
Brain Cortex ◽  
Post Traumatic Stress ◽  
Model Following ◽  
Initial Injury ◽  
Initial Activation ◽  
Post Traumatic ◽  
Oligodendrocyte Precursor ◽  
The Brain

Neurological manifestations of blast-induced Post Traumatic Stress Disorder (PTSD) extend long after the initial injury indicating lasting changes in brain function. In this study, we characterized brain injury, changes in neurogenesis and oligodendrogenesis in an adult murine blast model following a short (5 days) and long (21 days) post-blast recovery. Acoustic blasts led to an initial, activation of microglia and astrogliosis and a widespread cortical and subcortical apoptosis. The loss of myelinated cortical axons at 5 days was followed by the reappearance of abnormal misdirected fibers at 21 days. At 21 days post-blast, we observed increases in doublecortin-positive (DCX+ ) neuroblasts in the subventricular zone (SVZ) and hippocampal subgranular zone (SGZ) indicating increased neurogenesis. No changes in DCX+ cells were found in the brain cortex. In the cortex, the early disappearance of myelinated neuronal fibers was accompanied by a loss of O4+ oligodendrocytes and their Ki67-expreasing (Ki67+ ) oligodendrocyte precursor cells (OPC). However, at 5 days we observed a robust appearance of cells expressing Olig2 (O2+ ), an early determinant of oligodendrocyte lineage. At 21 days post-blast, the population of OPC increased and the mature O4+ oligodendrocytes were restored to control levels. In contrast, in the SVZ and SGZ, O4+ cells were not affected by the blast suggesting a local cortical origin for cortical oligodendrogenesis. These results suggest that blast-induced activation of SVZ and SGZ neurogenesis and cortical oligodendrogenesis could have long-lasting impact on brain function including memory disorders observed in both animal models and human’s PTSD.

scholarly journals Differential Diagnosis of the Dementias of Unknown Origin: A Clinician's View

1986 ◽  
Vol 13 (S4) ◽  
pp. 381-382 ◽  
Author(s):  
V.A. Kral
Keyword(s):  
Rural Areas ◽  
Unknown Origin ◽  
Brain Parenchyma ◽  
Laboratory Research ◽  
Cerebral Vasculature ◽  
Pathogenetic Mechanism ◽  
Number Of Patients ◽  
Life Threatening ◽  
Close Cooperation ◽  
The Brain

Abstract:The close cooperation of clinical and laboratory research has helped to clarify the etiology of some of the dementing processes of the senium. However, the necessary investigations are complicated, laborious, expensive and can be carried out only in well equipped centres in larger cities. This restricts the number of patients who eventually may benefit from these investigations to a small number. What is needed for the psychogeriatric practice particularly in rural areas and smaller cities are simple diagnostic guidelines for the psychiatrist to answer the question whether the patient suffers from a dementia and if so whether the dementia is in all probability due to a primary degenerative process of the brain parenchyma or of the cerebral vasculature or is it due to another cause.If degeneration of the brain parenchyma seems the prevalent pathogenetic mechanism one would like to establish in a given case which of the known degenerative processes is most probably present in order to avoid mistakes in clinical judgement with their often life threatening consequences.

scholarly journals Adenosine kinase inhibition promotes proliferation of neural stem cells after traumatic brain injury

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Hoda M Gebril ◽  
Rizelle Mae Rose ◽  
Raey Gesese ◽  
Martine P Emond ◽  
Yuqing Huo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Brain Injury ◽  
Neural Stem Cell ◽  
Adenosine Kinase ◽  
Health Concern ◽  
Stem Cell Proliferation ◽  
Neural Stem Cell Proliferation ◽  
The Brain

Abstract Traumatic brain injury (TBI) is a major public health concern and remains a leading cause of disability and socio-economic burden. To date, there is no proven therapy that promotes brain repair following an injury to the brain. In this study, we explored the role of an isoform of adenosine kinase expressed in the cell nucleus (ADK-L) as a potential regulator of neural stem cell proliferation in the brain. The rationale for this hypothesis is based on coordinated expression changes of ADK-L during foetal and postnatal murine and human brain development indicating a role in the regulation of cell proliferation and plasticity in the brain. We first tested whether the genetic disruption of ADK-L would increase neural stem cell proliferation after TBI. Three days after TBI, modelled by a controlled cortical impact, transgenic mice, which lack ADK-L (ADKΔneuron) in the dentate gyrus (DG) showed a significant increase in neural stem cell proliferation as evidenced by significant increases in doublecortin and Ki67-positive cells, whereas animals with transgenic overexpression of ADK-L in dorsal forebrain neurons (ADK-Ltg) showed an opposite effect of attenuated neural stem cell proliferation. Next, we translated those findings into a pharmacological approach to augment neural stem cell proliferation in the injured brain. Wild-type C57BL/6 mice were treated with the small molecule adenosine kinase inhibitor 5-iodotubercidin for 3 days after the induction of TBI. We demonstrate significantly enhanced neural stem cell proliferation in the DG of 5-iodotubercidin-treated mice compared to vehicle-treated injured animals. To rule out the possibility that blockade of ADK-L has any effects in non-injured animals, we quantified baseline neural stem cell proliferation in ADKΔneuron mice, which was not altered, whereas baseline neural stem cell proliferation in ADK-Ltg mice was enhanced. Together these findings demonstrate a novel function of ADK-L involved in the regulation of neural stem cell proliferation after TBI.

scholarly journals Penetrating brain injury with a metal bar and a knife: Report of two interesting cases

2017 ◽  
Vol 31 (2) ◽  
pp. 203-206 ◽  
Author(s):  
Alireza Tabibkhooei ◽  
Morteza Taheri ◽  
Sadra Rohani ◽  
Iran Chanideh ◽  
Hessam Rahatlou
Keyword(s):  
Brain Injury ◽  
Surgical Intervention ◽  
Wide Spectrum ◽  
Good Health ◽  
Brain Parenchyma ◽  
Antibiotic Administration ◽  
Case Presentation ◽  
Penetrating Brain Injury ◽  
Magnetic Resonance Imaging Mri ◽  
The Brain

Introduction Penetrating brain injury (PBI) is uncommon among the civilian population. Here, we report two interesting cases of PBI. Case presentation The first patient was a 20-year-old male who sustained a penetrating head injury with a metal bar during an accident at work. The patient underwent early surgical intervention, and related meningitis was treated with antibiotics. The patient was discharged 45 days later with no deficit. The second patient was a 34-year-old male who was the victim of a violence attack and was admitted to hospital. He was struck by a knife to his right temporal bone. A brain computed tomography scan and magnetic resonance imaging (MRI) demonstrated the tract of the knife within the brain parenchyma. The patient underwent conservative treatment. After several weeks, the patient was discharged in good health. Conclusion Although severe PBI has a poorer prognosis than a blunt brain injury, in treating of these patients, aggressive and timely surgical intervention, proper wide-spectrum antibiotic administration, stringent and diligent care in the intensive-care unit and careful management of the associated complications are mandated.

scholarly journals Immunological context of brain injury

2021 ◽  
Vol 23 (1) ◽  
pp. 163-168
Author(s):  
N. G. Plekhova ◽  
I. V. Radkov ◽  
S. V. Zinoviev ◽  
V. B. Shumatov
Keyword(s):  
Traumatic Brain Injury ◽  
T Cells ◽  
Brain Injury ◽  
Positive Reaction ◽  
Mild Traumatic Brain Injury ◽  
Brain Parenchyma ◽  
Post Injury ◽  
Blood Leukocytes ◽  
Subsequent Decrease ◽  
The Brain

The parameters of several populations of immune cells (T cell populations, macrophage subpopulations) in peripheral blood and brain were studied in a clinically significant model of mild traumatic brain injury among rats. The population of resident cells of innate immunity of microglia and brain astrocytes with local tissue damage is involved in the implementation of the inflammatory response, it is also shown that in case of trauma, blood leukocytes can overcome the blood-brain barrier and penetrate the brain parenchyma. The methods of flow cytometry and immunofluorescence were used. An increase in the number of monocytes and neutrophils up to 1 day, after a mild traumatic brain injury (TBI) with a subsequent decrease to the end of the observation period was noticed. It was determined, that the number of CD45+ cells, CD3+T cells decreased at 1 days post-injury (dpi), and rose slightly by 14 dpi, the percentage of CD4+T cells continuously declined from 7 to 14 dpi, while the percentage of CD8+T cells increased from 7 to 14 dpi. With mild traumatic brain injury in animals, a significant (3-10 times) decrease in the number of microvessels with a positive reaction to the presence of SMI 71 on the 8th and 14th day after head injury was observed. Intensive staining of SMI 71 microvessels was sometimes observed with an increase in the area of a positive reaction. Thin positive deposits of the reaction product are observed in the brain of healthy animals around the wall of the microvessel. In the damaged brain, CD45high/CD11b+ positive macrophages of the M1 subpopulation appeared in the brain tissue on the 2nd day after TBI and a significant amount was observed on the 8-14th day. In the corpus callosum and ipsilateral region of the striatum, the content of cells expressing CD16/11b+ reached a maximum 8 days after TBI, which correlated with a decrease in the positive response to the presence of endothelial antigen SMI 71. Thus, in the acute period of mild TBI, the presence of neuroimmunopathological processes is determined in the brain, which can subsequently result to the dysregulation of neuroimmune connections.

scholarly journals Does Blast Exposure to the Torso Cause a Blood Surge to the Brain?

2020 ◽  
Vol 8 ◽  
Author(s):  
Jose E. Rubio ◽  
Maciej Skotak ◽  
Eren Alay ◽  
Aravind Sundaramurthy ◽  
Dhananjay Radhakrishnan Subramaniam ◽  
...  
Keyword(s):  
Brain Injury ◽  
Carotid Artery ◽  
Brain Tissue ◽  
Shear Stresses ◽  
Fe Model ◽  
Cerebral Vasculature ◽  
Blast Exposure ◽  
Indirect Mechanism ◽  
Wall Shear ◽  
The Brain

The interaction of explosion-induced blast waves with the torso is suspected to contribute to brain injury. In this indirect mechanism, the wave-torso interaction is assumed to generate a blood surge, which ultimately reaches and damages the brain. However, this hypothesis has not been comprehensively and systematically investigated, and the potential role, if any, of the indirect mechanism in causing brain injury remains unclear. In this interdisciplinary study, we performed experiments and developed mathematical models to address this knowledge gap. First, we conducted blast-wave exposures of Sprague-Dawley rats in a shock tube at incident overpressures of 70 and 130 kPa, where we measured carotid-artery and brain pressures while limiting exposure to the torso. Then, we developed three-dimensional (3-D) fluid-structure interaction (FSI) models of the neck and cerebral vasculature and, using the measured carotid-artery pressures, performed simulations to predict mass flow rates and wall shear stresses in the cerebral vasculature. Finally, we developed a 3-D finite element (FE) model of the brain and used the FSI-computed vasculature pressures to drive the FE model to quantify the blast-exposure effects in the brain tissue. The measurements from the torso-only exposure experiments revealed marginal increases in the peak carotid-artery overpressures (from 13.1 to 28.9 kPa). Yet, relative to the blast-free, normotensive condition, the FSI simulations for the blast exposures predicted increases in the peak mass flow rate of up to 255% at the base of the brain and increases in the wall shear stress of up to 289% on the cerebral vasculature. In contrast, our simulations suggest that the effect of the indirect mechanism on the brain-tissue-strain response is negligible (<1%). In summary, our analyses show that the indirect mechanism causes a sudden and abundant stream of blood to rapidly propagate from the torso through the neck to the cerebral vasculature. This blood surge causes a considerable increase in the wall shear stresses in the brain vasculature network, which may lead to functional and structural effects on the cerebral veins and arteries, ultimately leading to vascular pathology. In contrast, our findings do not support the notion of strain-induced brain-tissue damage due to the indirect mechanism.

Abstract 13824: Computerized Tomography vs Ultrasound Imaging for Detecting Hypoxic-Ischemic Brain Injury

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Benjamin Karfunkle ◽  
Pavitra Kotini-shah ◽  
Richard Gordon ◽  
Jing Li ◽  
Misha Granado ◽  
...  
Keyword(s):  
Brain Injury ◽  
Hospital Discharge ◽  
Computerized Tomography ◽  
Point Of Care ◽  
Ischemic Injury ◽  
Ct Head ◽  
Ct Brain ◽  
Initial Imaging ◽  
The Brain ◽  
Hypoxic Ischemic Injury

Introduction: After an out-of-hospital cardiac arrest (OHCA), the resulting hypoxic-ischemic injury (HII) to the brain remains the main cause of mortality. Standardized approaches for measuring the extent of injury and monitoring of changes are lacking and continue to be a critical barrier to progress in improving neurological survival. Objective: We sought to characterize the prevalence of HII detected on computerized tomography of the brain and its correlation to point-of-care optic nerve sheath diameter (ONSD) measurements as an alternative modality for detecting brain injury. Methods: Adult OHCA patients at an urban academic ED were included in this study on a convenience sample basis from 2018-2019. The patients were grouped by findings of hypoxic-ischemic injury (HII) on both initial and subsequent CT brain imaging performed after ROSC in respective groups. CT Brain findings were compared to ONSD measurements as performed with point-of-care ultrasound by fellowship-trained emergency physicians within one hour of hospital arrival and at 6 hours, after return of spontaneous circulation (ROSC) and to cerebral performance category (CPC) at hospital discharge. Results: 76 patients enrolled in the study had a median age was 59, 49% were female, and 37% survived to hospital discharge. 58 patients had CT head performed, 40 had ONSD measured within one hour, and 27 patients had both. Of that 27, 9 (33%) had evidence of HII on initial imaging and 15 (55%) had evidence of HII on subsequent imaging for a total of 20 unique patients. The average ONSD within 1 hour of ROSC for those with no HII on any imaging was 0.59 cm, and for those without HII on initial imaging but with HII on subsequent imaging was 0.67 cm, and this difference was statistically significant (p< 0.05). Of the 20 patients with HI, 14 (70%) patients died and 6 (30%) survived with a CPC of 4. The average time to first CT head was 4 hours and 45 mins and the average time to subsequent imaging was 97 hours and 45 mins. Conclusion: After an OHCA, early time point ONSD measurements can potentially indicate brain injury within 1 hour of ROSC even in those without initial evidence of HII on CT imaging.

scholarly journals Relevance of Blood Vessel Networks in Blast-Induced Traumatic Brain Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Yi Hua ◽  
Shengmao Lin ◽  
Linxia Gu
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Blood Vessel ◽  
Vessel Diameter ◽  
Dynamic Responses ◽  
Brain Dynamics ◽  
Cerebral Vasculature ◽  
Vessel Networks ◽  
The Brain

Cerebral vasculature is a complex network that circulates blood through the brain. However, the role of this networking effect in brain dynamics has seldom been inspected. This work is to study the effects of blood vessel networks on dynamic responses of the brain under blast loading. Voronoi tessellations were implemented to represent the network of blood vessels in the brain. The brain dynamics in terms of maximum principal strain (MPS), shear strain (SS), and intracranial pressure (ICP) were monitored and compared. Results show that blood vessel networks significantly affected brain responses. The increased MPS and SS were observed within the brain embedded with vessel networks, which did not exist in the case without blood vessel networks. It is interesting to observe that the alternation of the ICP response was minimal. Moreover, the vessel diameter and density also affected brain dynamics in both MPS and SS measures. This work sheds light on the role of cerebral vasculature in blast-induced traumatic brain injury.

Cerebrovascular Dysfunction Following Sub-Failure Axial Stretch

2013 ◽  
Author(s):  
E. David Bell ◽  
Kenneth L. Monson
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Autoregulation ◽  
Mechanical Damage ◽  
Cerebral Vasculature ◽  
Cerebral Blood Vessels ◽  
Axial Stretch ◽  
Cerebrovascular Dysfunction ◽  
And Function ◽  
The Brain

Cerebral blood vessels are critical in maintaining the health and function of the brain, but their function can be disrupted by traumatic brain injury (TBI), which commonly includes damage to these vessels [1]. However, even in cases where there is not apparent mechanical damage to the cerebral vasculature, TBI can induce physiological disruptions that can lead to breakdown of the blood brain barrier or loss of cerebral autoregulation.

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