scholarly journals Cognitive Recovery and Rehabilitation After Brain Injury: Mechanisms, Challenges and Support

10.5772/28242 ◽  
2012 ◽  
Author(s):  
Jesper Mogensen
Keyword(s):  
Brain Injury ◽  
Cognitive Recovery ◽  
Injury Mechanisms

scholarly journals Fine Tuning of Traumatic Brain Injury Management in Neurointensive Care—Indicative Observations and Future Perspectives

2021 ◽  
Vol 12 ◽  
Author(s):  
Teodor M. Svedung Wettervik ◽  
Anders Lewén ◽  
Per Enblad
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Fine Tuning ◽  
Neurointensive Care ◽  
Secondary Brain Injury ◽  
Brain Tissue Oxygenation ◽  
Treatment Protocols ◽  
Injury Mechanisms ◽  
Severe Tbi ◽  
Type Of Injury

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.

The Use of a Cellular Strain Injury Criterion and Diffusion Tensor Imaging in a Computational Model of Traumatic Brain Injury

2010 ◽  
Author(s):  
Rika M. Wright ◽  
K. T. Ramesh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mechanical Loading ◽  
Computational Models ◽  
Diffusion Tensor ◽  
Diffuse Axonal Injury ◽  
Element Model ◽  
Cellular Level ◽  
Cellular Injury ◽  
Injury Mechanisms

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.

Blast Traumatic Brain Injury Mechanisms

Neurotrauma ◽  
2018 ◽  
pp. 111-122
Author(s):  
Elizabeth McNeil ◽  
Zachary Bailey ◽  
Allison Guettler ◽  
Pamela VandeVord
Keyword(s):  
Traumatic Brain Injury ◽  
Finite Element ◽  
Brain Injury ◽  
Head Injury ◽  
Mechanism Of Injury ◽  
Primary Blast ◽  
Blast Traumatic Brain Injury ◽  
Injury Mechanisms ◽  
Biomechanical Investigation

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.

Branched-Chain Amino Acids Enhance the Cognitive Recovery of Patients With Severe Traumatic Brain Injury

2005 ◽  
Vol 86 (9) ◽  
pp. 1729-1735 ◽  
Author(s):  
Roberto Aquilani ◽  
Paolo Iadarola ◽  
Antonella Contardi ◽  
Mirella Boselli ◽  
Manuela Verri ◽  
...  
Keyword(s):  
Amino Acids ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Branched Chain Amino Acids ◽  
Cognitive Recovery ◽  
Branched Chain

Methodological Issues in Longitudinal Research on Cognitive Recovery after Traumatic Brain Injury: Evidence from a Systematic Review

2013 ◽  
Vol 14 (3) ◽  
pp. 450-474 ◽  
Author(s):  
Regina Schultz ◽  
Robyn L. Tate
Keyword(s):  
Systematic Review ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Longitudinal Research ◽  
Effect Sizes ◽  
Methodological Issues ◽  
Post Injury ◽  
Cognitive Recovery ◽  
Cognitive Domains ◽  
Severe Tbi

Background: Previous research addressing cognitive recovery after traumatic brain injury (TBI) in adults has predominately used cross-sectional methods. This systematic review examines longitudinal research into cognitive recovery in the first 2 years following moderate-to-severe TBI in adults and aims to identify apparent methodological issues with the existing literature.Design: Systematic review of the first 2 years post-trauma.Setting: Data were extracted from three electronic databases and manual searches of published articles until October 2012.Participants: Two hundred and forty-two participants with severe TBI and 281 comparison participants were used to calculate effect sizes.Results: Twenty papers met the selection criteria, with effect sizes computed from four studies. Moderate-to-large effect sizes were initially observed between the TBI and comparison groups on most measures (range: d = 0.2–2.8). Recovery continued in all five cognitive domains over the 2 years post-injury.Conclusions: Results demonstrated that cognitive recovery was continuous throughout the first 2 years following moderate-to-severe TBI. Findings also indicated different rates of recovery for the specific cognitive domains, highlighting the heterogeneous nature of cognitive recovery after TBI. The review highlighted several methodological issues within the limited existing literature; recommendations were developed to improve the evidence base.

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