A Translational Model of Traumatic Brain Injury: Sheep Impact Acceleration

Author(s):  
Robert Vink
2009 ◽  
Vol 30 (3) ◽  
pp. 628-637 ◽  
Author(s):  
Guoyi Gao ◽  
Yasutaka Oda ◽  
Enoch P Wei ◽  
John T Povlishock

This study examined the effect of posttraumatic hypoxia on cerebral vascular responsivity and axonal damage, while also exploring hypothermia's potential to attenuate these responses. Rats were subjected to impact acceleration injury (IAI) and equipped with cranial windows to assess vascular reactivity to topical acetylcholine, with postmortem analyses using antibodies to amyloid precursor protein to assess axonal damage. Animals were subjected to hypoxia alone, IAI and hypoxia, IAI and hypoxia before induction of moderate hypothermia (33°C), IAI and hypoxia induced during hypothermic intervention, and IAI and hypoxia initiated after hypothermia. Hypoxia alone had no impact on vascular reactivity or axonal damage. Acceleration injury and posttraumatic hypoxia resulted in dramatic axonal damage and altered vascular reactivity. When IAI and hypoxia were followed by hypothermic intervention, no axonal or vascular protection ensued. However, when IAI was followed by hypoxia induced during hypothermia, axonal and vascular protection followed. When this same hypoxic insult followed the use of hypothermia, no benefit ensued. These studies show that early hypoxia and delayed hypoxia exert damaging axonal and vascular consequences. Although this damage is attenuated by hypothermia, this follows only when hypoxia occurs during hypothermia, with no benefit found if the hypoxic insult proceeds or follows hypothermia.


2004 ◽  
Vol 140 (1-2) ◽  
pp. 23-28 ◽  
Author(s):  
Emilie Carré ◽  
Emmanuel Cantais ◽  
Olivier Darbin ◽  
Jean-Pierre Terrier ◽  
Michel Lonjon ◽  
...  

PM&R ◽  
2016 ◽  
Vol 8 (9) ◽  
pp. S227
Author(s):  
Scott Barbay ◽  
Hongyu Zhang ◽  
Shawn B. Frost ◽  
Jeremy C. Peterson ◽  
David J. Guggenmos ◽  
...  

2001 ◽  
Vol 18 (6) ◽  
pp. 607-614 ◽  
Author(s):  
Richard H. Singleton ◽  
James R. Stone ◽  
David O. Okonkwo ◽  
Anthony J. Pellicane ◽  
John T. Povlishock

2005 ◽  
Vol 103 (4) ◽  
pp. 707-714 ◽  
Author(s):  
Michael F. Stiefel ◽  
Yoshiyuki Tomita ◽  
Anthony Marmarou

Object. It is well established that posttraumatic secondary ischemia contributes to poor outcome. Ion dysfunction leading to cytotoxic edema is a primary force in the formation of ischemic brain edema and is a principal component of traumatic brain swelling. Because cell swelling is the result of net ion and water movement, it is crucial to have a thorough understanding of these transient phenomena. The purpose of this study was to characterize the effects of secondary ischemia following traumatic brain injury (TBI) on the ability to restore ion homeostasis. Methods. Twenty-four Sprague—Dawley rats were divided into four groups of six animals each. The rats underwent transient forebrain ischemia via bilateral carotid artery occlusion combined with hypotension: 15 minutes of forebrain ischemia (Group 1); 60 minutes of forebrain ischemia (Group 2); impact acceleration/TBI (Group 3); and impact acceleration/TBI followed by 15 minutes of ischemia (Group 4). Ischemia resulted in a rapid accumulation of [K+]e: 41.94 ± 13.65 and 66.33 ± 6.63 mM, respectively, in Groups 1 and 2, with a concomitant decrease of [Na+]e: 64 ± 18 mM and 72 ± 11 mM in Groups 1 and 2. Traumatic brain injury resulted in a less severe although identical trend in ion dysfunction ([K+]e 30.42 ± 11.67 mM and [Na+]e 63 ± 33 mM). Secondary ischemia resulted in prolonged and sustained ion dysfunction with a concomitant elevation of intracranial pressure (ICP). Conclusions. Analysis of these results indicates that ischemia and TBI are sublethal in isolation; however, when TBI is associated with secondary ischemia, ion dysfunction is sustained and is associated with elevated ICP.


Author(s):  
Sarah C. Hellewell ◽  
Jenna M. Ziebell ◽  
Jonathan Lifshitz ◽  
M. Cristina Morganti-Kossmann

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.


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.


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