scholarly journals Traumatic cerebral contusion: pathobiology and critical aspects

2013 ◽  
Vol 20 (2) ◽  
pp. 125-137
Author(s):  
Hernando Alvis-Miranda ◽  
Gabriel Alcala-Cerra ◽  
Luis Rafael Moscote-Salazar

AbstractTraumatic brain injury is a major cause of mortality in developed countries. Cerebral parenchymal injury is evidenced by a significant percentage of patients. The most important structural lesion of the brain is the cerebral contusion, which is a complex and dynamic area, a result of the primary lesion and which is associated with ischemic and inflammatory phenomena that need to be known by the neurosurgeon. We present a review of the most important aspects of brain contusion.

2016 ◽  
Vol 9 ◽  
pp. CCRep.S40607 ◽  
Author(s):  
Tetsu Akimoto ◽  
Tomoyuki Yamazaki ◽  
Eiji Kusano ◽  
Daisuke Nagata

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.


2021 ◽  
Vol 23 (4) ◽  
pp. 825-830
Author(s):  
A. O. Norka ◽  
S. V. Vorobyev ◽  
R. N. Kuznetsova ◽  
M. K. Serebriakova ◽  
I. V. Kudryavtsev ◽  
...  

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. 


2020 ◽  
Vol 25 (11) ◽  
pp. 283-288
Author(s):  
Mark Lowrie

Traumatic brain injury occurs frequently in dogs and cats. The primary lesion occurs at the time of injury and causes direct, irreversible damage to the brain parenchyma and vasculature. Secondary lesions occur in the minutes following the trauma as a result of a combination of physical and biochemical changes that lead to intracranial hypertension. It is this secondary injury that veterinarians are able to reduce. This article outlines the treatment options for patients with traumatic brain injury. There remains controversy over what constitutes best practice. This article addresses the main points regarding the clinical therapeutic options currently available.


2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy

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.


2018 ◽  
pp. 110-119

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.


2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou

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.


2021 ◽  
Vol 7 (10) ◽  
pp. eabe0207
Author(s):  
Charles-Francois V. Latchoumane ◽  
Martha I. Betancur ◽  
Gregory A. Simchick ◽  
Min Kyoung Sun ◽  
Rameen Forghani ◽  
...  

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.


CNS Spectrums ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 178-179
Author(s):  
John L. Sherman ◽  
Laurence J. Adams ◽  
Christen F. Kutz ◽  
Deborah York ◽  
Mitchell S. Szymczak

AbstractTraumatic brain injury (TBI) is a complex phenomenon affecting multiple areas of the brain in multiple ways. Both right and left hemispheres are affected as well as supratentorial and infratentorial compartments. These multifocal injuries are caused by many factors including acute mechanical injury, focal intracranial hemorrhage, blunt and rotational forces, epidural and subdural hematoma, hypoxemia, hypotension, edema, axonal damage, neuronal death, gliosis and blood brain barrier disruption. Clinicians and patients benefit by precise information about the neuroanatomical areas that are affected macroscopically, microscopically and biochemically in an individual patient.Standard imaging studies are frequently negative or grossly underestimate the severity of TBI and may exacerbate and prolong patient suffering with an imaging result of “no significant abnormality”. Specifically, sophisticated imaging tools have been developed which reveal significant damage to the brain structure including atrophy, MRI spectroscopy showing variations in neuronal metabolite N-acetyl-aspartate, elevations of membrane related Choline, and the glial metabolite myo-inositol is often observed to be increased post injury. In addition, susceptibility weighted imaging (SWI) has been shown to be more reliable for detecting microbleeds versus calcifications.We have selected two TBI patients with diffuse traumatic brain injury.The first patient is a 43-year-old male who suffered severe traumatic brain injury from a motorcycle accident in 2016. Following the accident, the patient was diagnosed with seizures, major depression, and intermittent explosive disorder. He has attempted suicide and has neurobehavioral disinhibition including severe anger, agitation and irritability. He denies psychiatric history prior to TBI and has negative family history. Following the TBI, he became physically aggressive and assaultive in public with minimal provocation. He denies symptoms of thought disorder and mania. He is negative for symptoms of  cognitive decline or encephalopathy.The second patient is a 49-year-old male who suffered at least 3 concussive blasts in the Army and a parachute injury. Following the last accident, the patient was diagnosed with major depressive disorder, panic disorder, PTSD and generalized anxiety disorder. He denies any psychiatric history prior to TBI including negative family history of psychiatric illness. In addition, he now suffers from nervousness, irritability, anger, emotional lability and concurrent concentration issues, problems completing tasks and alterations in memory.Both patients underwent 1.5T multiparametric MRI using standard T2, FLAIR, DWI and T1 sequences, and specialized sequences including susceptibility weighted (SWAN/SWI), 3D FLAIR, single voxel MRI spectroscopy (MRS), diffusion tensor imaging (DTI), arterial spin labeling perfusion (ASL) and volumetric MRI (NeuroQuant). Importantly, this exam can be performed in 30–45 minutes and requires no injections other than gadolinium in some patients. We will discuss the insights derived from the MRI which detail the injured areas, validate the severity of the brain damage, and provide insight into the psychological, motivational and physical disabilities that afflict these patients. It is our expectation that this kind of imaging study will grow in value as we link specific patterns of injury to specific symptoms and syndromes resulting in more targeted therapies in the future.


Sign in / Sign up

Export Citation Format

Share Document