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.

Biaxial and Failure Mechanical Properties of Passive Rat Middle Cerebral Arteries

2011 ◽  
Author(s):  
E. David Bell ◽  
Rahul S. Kunjir ◽  
Kenneth L. Monson
Keyword(s):  
Mechanical Properties ◽  
Traumatic Brain Injury ◽  
Cerebral Autoregulation ◽  
Cerebral Arteries ◽  
Mechanical Damage ◽  
Cerebral Vasculature ◽  
Cerebral Blood Vessels ◽  
Middle Cerebral Arteries ◽  
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.

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.

Simulation of Blast-Head Interactions to Study Traumatic Brain Injury

2007 ◽  
Author(s):  
M. Sotudeh Chafi ◽  
G. Karami ◽  
M. Ziejewski
Keyword(s):  
Traumatic Brain Injury ◽  
Shear Stress ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Stress Responses ◽  
Maximum Shear Stress ◽  
Mechanical Damage ◽  
Shock Propagation ◽  
Arbitrary Lagrangian Eulerian ◽  
The Brain

This paper presents a methodology for predicting the mechanical damage inflicted on the brain by a high explosive (HE) detonation and leading to traumatic brain injury (TBI). A brain model, with its complexity, is used in the computational procedure. The processes of HE detonation and shock propagation in the air, as well as their interaction with the head, are modeled by an Arbitrary Lagrangian Eulerian (ALE) multi-material formulation, together with a penalty-based fluid/structure interaction algorithm. This methodology provides intracranial pressure and maximum shear stress within the microscale time frame for this highly dynamic phenomenon. Two scenarios are simulated. In one scenario, the brain is in close proximity to a 1lb trinitrotoluene (TNT) explosion, and the other to a 0.5lb explosion. The resulting countercoup intracranial pressure-time histories, from the 1 lb TNT explosive scenario, demonstrates that pressure falls below −100 kPa. This can cause cavitation bubbles and damage to the brain tissue. The simulations also predict that the areas of high pressure and shear stress concentration are consistent with those of clinical observations. These resulted intracranial pressure and shear stress responses are the parameters to examine against injury criterions thresholds.

scholarly journals A Multiscale Model of Traumatic Brain Injury Suggests Possible Mechanisms of Post-Traumatic Psychosis

2021 ◽  
Author(s):  
Dalton A R Sakthivadivel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Traumatic Injury ◽  
Multiscale Model ◽  
Cortical Activation ◽  
Post Injury ◽  
Regulation Of Activity ◽  
Post Traumatic ◽  
And Function ◽  
The Brain

AbstractTraumatic brain injury is a devastating injury to the brain that can have permanent or fatal effects, leading to life-long deficits or death. Among these effects is psychosis and schizophrenia, sometimes reported in the population of TBI sufferers. Here we evaluate a possible mechanism of post-traumatic psychosis, shedding light on the anomalous nature of psychosis as over-activity and brain injury as destruction. Using a multiscale model of the brain to relate molecular pathology to connectomic and macroscopic features of the brain, we identify cell lysis and membrane deformation as a possible mechanism for psychosis after injury. We also evaluate the reorganisation of functional networks and cortical activation post-injury, and find the features of a simulated brain under traumatic injury correlate with recorded results on the schizophrenic functional connectome. This provides a possible mechanism for post-traumatic psychosis, as well as a proof-of-principle of advanced multiscale modelling methods in computational psychiatry and neuromedicine. It also elaborates on the relationship between structure and function in the brain, information processing, and the delicate regulation of activity in healthy brains.

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 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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