scholarly journals Modeling traumatic brain injury: mechanisms of early neuronal and axon degeneration in the infant rodent brain

2019 ◽  
Vol 30 (0) ◽  
pp. 25
Author(s):  
Krikor Dikranian
2021 ◽  
Vol 12 ◽  
Author(s):  
Teodor M. Svedung Wettervik ◽  
Anders Lewén ◽  
Per Enblad

Neurointensive care (NIC) has contributed to great improvements in clinical outcomes for patients with severe traumatic brain injury (TBI) by preventing, detecting, and treating secondary insults and thereby reducing secondary brain injury. Traditional NIC management has mainly focused on generally applicable escalated treatment protocols to avoid high intracranial pressure (ICP) and to keep the cerebral perfusion pressure (CPP) at sufficiently high levels. However, TBI is a very heterogeneous disease regarding the type of injury, age, comorbidity, secondary injury mechanisms, etc. In recent years, the introduction of multimodality monitoring, including, e.g., pressure autoregulation, brain tissue oxygenation, and cerebral energy metabolism, in addition to ICP and CPP, has increased the understanding of the complex pathophysiology and the physiological effects of treatments in this condition. In this article, we will present some potential future approaches for more individualized patient management and fine-tuning of NIC, taking advantage of multimodal monitoring to further improve outcome after severe TBI.


Author(s):  
Rika M. Wright ◽  
K. T. Ramesh

With the increase in the number of soldiers sustaining traumatic brain injury from military incidents and the recent attention on sports related traumatic brain injury, there has been a focused effort to develop preventative and treatment methods for traumatic brain injury (TBI). Traumatic brain injury is caused by mechanical loading to the head, such as from impacts, sudden accelerations, or blast loading, and the pathology can range from focal damage in the brain to widespread diffuse injury [1]. In this study, we investigate the injury mechanisms of diffuse axonal injury (DAI), which accounts for the second largest percentage of deaths due to brain trauma [2]. DAI is caused by sudden inertial loads to the head, and it is characterized by damage to neural axons. Despite the extensive research on DAI, the coupling between the mechanical loading to the head and the damage at the cellular level is still poorly understood. Unlike previous computational models that use macroscopic stress and strain measures to determine injury, a cellular injury criterion is used in this work as numerous studies have shown that cellular strain can be related to the functional damage of neurons. The effectiveness of using this cellular injury criterion to predict damage in a finite element model of DAI is investigated.


Neurotrauma ◽  
2018 ◽  
pp. 111-122
Author(s):  
Elizabeth McNeil ◽  
Zachary Bailey ◽  
Allison Guettler ◽  
Pamela VandeVord

Blast traumatic brain injury (bTBI) is a leading cause of head injury in soldiers returning from the battlefield. Primary blast brain injury remains controversial with little evidence to support a primary mechanism of injury. The four main theories described herein include blast wave transmission through skull orifices, direct cranial transmission, thoracic surge, and skull flexure dynamics. It is possible that these mechanisms do not occur exclusively from each other, but rather that several of them lead to primary blast brain injury. Biomechanical investigation with in-vivo, cadaver, and finite element models would greatly increase our understanding of bTBI mechanisms.


2013 ◽  
Vol 30 (1) ◽  
pp. 30-38 ◽  
Author(s):  
Mayumi L. Prins ◽  
Daya Alexander ◽  
Christopher C. Giza ◽  
David A. Hovda

Author(s):  
Jiangyue Zhang ◽  
Narayan Yoganandan ◽  
Frank A. Pintar ◽  
Steven F. Son ◽  
Thomas A. Gennarelli

Traumatic brain injury from explosive devices has become the signature wound of the U.S. armed forces in Iraq and Afghanistan [1–4]. However, due to the complicated nature of this specific form of brain injury, little is known about the injury mechanisms. Physical head models have been used in blunt and penetrating head trauma studies to obtain biomechanical data and correlate to mechanisms of injury [5–8]. The current study is designed to investigate intracranial head/brain injury biomechanics under blast loading using a physical head model.


2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Zunjia Wen ◽  
Dong Li ◽  
Meifen Shen ◽  
Gang Chen

Massive studies have focused on the understanding of the pathobiology of cellular and molecular changes and injury mechanisms after traumatic brain injury (TBI), but very few studies have specially discussed the role of synapses in the context of TBI. This paper specifically highlights the role and therapeutic potentials of synapses after TBI. First, we review and conclude how synapses interact with constant structural, metabolic, neuroendocrine, and inflammatory mechanisms after TBI. Second, we briefly describe several key synaptic proteins involved in neuroplasticity, which may be novel neuronal targets for specific intervention. Third, we address therapeutic interventions in association with synapses after TBI. Finally, we concisely discuss the study gaps in the synapses after TBI, in hopes that this would provide more insights for future studies. Synapses play an important role in TBI; while the understandings on the synaptic participation in the treatments and prognosis of TBI are lacking, more studies in this area are warranted.


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