Head trauma: treatment and diagnostic aids

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.

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Traumatic brain injury in dogs and cats: a systematic review

Veterinární Medicína ◽

10.17221/20/2017-vetmed ◽

2018 ◽

Vol 63 (No. 8) ◽

pp. 345-357 ◽

Cited By ~ 4

Author(s):

LO Dos Santos ◽

GG Caldas ◽

CRO Santos ◽

DB Junior

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Motor Vehicle ◽

Brain Parenchyma ◽

Irreversible Damage ◽

Vehicle Accidents ◽

Secondary Damage ◽

Therapeutic Measures ◽

Crush Injuries ◽

The Brain

Traumatic brain injury occurs frequently in dogs and cats due to motor vehicle accidents, falls and crush injuries. 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 due to a combination of physical and biochemical changes that lead to intracranial hypertension. Therefore, knowing the pathophysiology of the cranioencephalic trauma is essential for treatment directed at minimising secondary damage. The approach to the patient affected by traumatic brain injury is based on the ABCD of trauma, guided by the neurological examination with the aid of imaging exams and adequate therapeutic measures. The treatment of patients with cranioencephalic trauma is still in many ways controversial. For that reason, this literature review aims to address the main points regarding the pathophysiology of this disease and to describe the clinical and surgical therapeutic options currently available.

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Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

Journal of Neurotrauma ◽

10.1089/neu.2013.2862 ◽

2013 ◽

Vol 30 (11) ◽

pp. 920-937 ◽

Cited By ~ 68

Author(s):

Patrick M. Kochanek ◽

C. Edward Dixon ◽

David K. Shellington ◽

Samuel S. Shin ◽

Hülya Bayır ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Molecular Mechanisms ◽

Secondary Injury ◽

Injury And Repair ◽

The Brain

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Immunological context of brain injury

Medical Immunology (Russia) ◽

10.15789/1563-0625-ico-2011 ◽

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.

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RhoA-ROCK Signaling as a Therapeutic Target in Traumatic Brain Injury

Cells ◽

10.3390/cells9010245 ◽

2020 ◽

Vol 9 (1) ◽

pp. 245 ◽

Cited By ~ 6

Author(s):

Shalaka Mulherkar ◽

Kimberley F. Tolias

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Traumatic Event ◽

Treatment Options ◽

Work Productivity ◽

Rho Kinase ◽

Small Gtpase ◽

Cns Injury ◽

Functional Impairments ◽

The Brain

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. TBIs, which range in severity from mild to severe, occur when a traumatic event, such as a fall, a traffic accident, or a blow, causes the brain to move rapidly within the skull, resulting in damage. Long-term consequences of TBI can include motor and cognitive deficits and emotional disturbances that result in a reduced quality of life and work productivity. Recovery from TBI can be challenging due to a lack of effective treatment options for repairing TBI-induced neural damage and alleviating functional impairments. Central nervous system (CNS) injury and disease are known to induce the activation of the small GTPase RhoA and its downstream effector Rho kinase (ROCK). Activation of this signaling pathway promotes cell death and the retraction and loss of neural processes and synapses, which mediate information flow and storage in the brain. Thus, inhibiting RhoA-ROCK signaling has emerged as a promising approach for treating CNS disorders. In this review, we discuss targeting the RhoA-ROCK pathway as a therapeutic strategy for treating TBI and summarize the recent advances in the development of RhoA-ROCK inhibitors.

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A Role for Nanoparticles in Treating Traumatic Brain Injury

Pharmaceutics ◽

10.3390/pharmaceutics11090473 ◽

2019 ◽

Vol 11 (9) ◽

pp. 473 ◽

Cited By ~ 9

Author(s):

Badrul Alam Bony ◽

Forrest M. Kievit

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Treatment Options ◽

Unmet Need ◽

Economic Loss ◽

Phase Iii ◽

Target Engagement ◽

Post Injury ◽

The Brain

Traumatic brain injury (TBI) is one of the main causes of disability in children and young adults, as well as a significant concern for elderly individuals. Depending on the severity, TBI can have a long-term impact on the quality of life for survivors of all ages. The primary brain injury can result in severe disability or fatality, and secondary brain damage can increase the complexities in cellular, inflammatory, neurochemical, and metabolic changes in the brain, which can last decades post-injury. Thus, survival from a TBI is often accompanied by lifelong disabilities. Despite the significant morbidity, mortality, and economic loss, there are still no effective treatment options demonstrating an improved outcome in a large multi-center Phase III trial, which can be partially attributed to poor target engagement of delivered therapeutics. Thus, there is a significant unmet need to develop more effective delivery strategies to overcome the biological barriers that would otherwise inhibit transport of materials into the brain to prevent the secondary long-term damage associated with TBI. The complex pathology of TBI involving the blood-brain barrier (BBB) has limited the development of effective therapeutics and diagnostics. Therefore, it is of great importance to develop novel strategies to target the BBB. The leaky BBB caused by a TBI may provide opportunities for therapeutic delivery via nanoparticles (NP). The focus of this review is to provide a survey of NP-based strategies employed in preclinical models of TBI and to provide insights for improved NP based diagnostic or treatment approaches. Both passive and active delivery of various NPs for TBI are discussed. Finally, potential therapeutic targets where improved NP-mediated delivery could increase target engagement are identified with the overall goal of providing insight into open opportunities for NP researchers to begin research in TBI.

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Coagulopathy induced by traumatic brain injury: systemic manifestation of a localized injury

Blood ◽

10.1182/blood-2017-11-784108 ◽

2018 ◽

Vol 131 (18) ◽

pp. 2001-2006 ◽

Cited By ~ 21

Author(s):

Jianning Zhang ◽

Fangyi Zhang ◽

Jing-fei Dong

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Clinical Outcomes ◽

Intracranial Hemorrhage ◽

Recent Progress ◽

Treatment Options ◽

Knowledge Gaps ◽

Systemic Manifestation ◽

The Brain

Abstract Traumatic brain injury (TBI)–induced coagulopathy is a common and well-recognized risk for poor clinical outcomes, but its pathogenesis remains poorly understood, and treatment options are limited and ineffective. We discuss the recent progress and knowledge gaps in understanding this lethal complication of TBI. We focus on (1) the disruption of the brain-blood barrier to disseminate brain injury systemically by releasing brain-derived molecules into the circulation and (2) TBI-induced hypercoagulable and hyperfibrinolytic states that result in persistent and delayed intracranial hemorrhage and systemic bleeding.

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Inflammatory Regulation of CNS Barriers After Traumatic Brain Injury: A Tale Directed by Interleukin-1

Frontiers in Immunology ◽

10.3389/fimmu.2021.688254 ◽

2021 ◽

Vol 12 ◽

Author(s):

Colleen N. Bodnar ◽

James B. Watson ◽

Emma K. Higgins ◽

Ning Quan ◽

Adam D. Bachstetter

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Immune Cells ◽

Interleukin 1 ◽

Brain Lesion ◽

The Body ◽

Future Research ◽

Secondary Injury ◽

Inflammatory Regulation ◽

The Brain

Several barriers separate the central nervous system (CNS) from the rest of the body. These barriers are essential for regulating the movement of fluid, ions, molecules, and immune cells into and out of the brain parenchyma. Each CNS barrier is unique and highly dynamic. Endothelial cells, epithelial cells, pericytes, astrocytes, and other cellular constituents each have intricate functions that are essential to sustain the brain’s health. Along with damaging neurons, a traumatic brain injury (TBI) also directly insults the CNS barrier-forming cells. Disruption to the barriers first occurs by physical damage to the cells, called the primary injury. Subsequently, during the secondary injury cascade, a further array of molecular and biochemical changes occurs at the barriers. These changes are focused on rebuilding and remodeling, as well as movement of immune cells and waste into and out of the brain. Secondary injury cascades further damage the CNS barriers. Inflammation is central to healthy remodeling of CNS barriers. However, inflammation, as a secondary pathology, also plays a role in the chronic disruption of the barriers’ functions after TBI. The goal of this paper is to review the different barriers of the brain, including (1) the blood-brain barrier, (2) the blood-cerebrospinal fluid barrier, (3) the meningeal barrier, (4) the blood-retina barrier, and (5) the brain-lesion border. We then detail the changes at these barriers due to both primary and secondary injury following TBI and indicate areas open for future research and discoveries. Finally, we describe the unique function of the pro-inflammatory cytokine interleukin-1 as a central actor in the inflammatory regulation of CNS barrier function and dysfunction after a TBI.

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Lessons Learned From Coaching Postsecondary Students With Traumatic Brain Injury

Perspectives of the ASHA Special Interest Groups ◽

10.1044/2019_persp-19-00092 ◽

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.

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