Impact Acceleration Model of Diffuse Traumatic Brain Injury

2016 ◽  
pp. 253-266 ◽  
Author(s):  
Sarah C. Hellewell ◽  
Jenna M. Ziebell ◽  
Jonathan Lifshitz ◽  
M. Cristina Morganti-Kossmann
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Acceleration Model ◽  
Impact Acceleration

The Immunophilin Ligand FK506 Attenuates Axonal Injury in an Impact-Acceleration Model of Traumatic Brain Injury

2001 ◽  
Vol 18 (6) ◽  
pp. 607-614 ◽  
Author(s):  
Richard H. Singleton ◽  
James R. Stone ◽  
David O. Okonkwo ◽  
Anthony J. Pellicane ◽  
John T. Povlishock
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Axonal Injury ◽  
Acceleration Model ◽  
Impact Acceleration

scholarly journals The Adverse Pial Arteriolar and Axonal Consequences of Traumatic Brain Injury Complicated by Hypoxia and Their Therapeutic Modulation with Hypothermia in Rat

2009 ◽  
Vol 30 (3) ◽  
pp. 628-637 ◽  
Author(s):  
Guoyi Gao ◽  
Yasutaka Oda ◽  
Enoch P Wei ◽  
John T Povlishock
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Amyloid Precursor Protein ◽  
Vascular Reactivity ◽  
Axonal Damage ◽  
Precursor Protein ◽  
Moderate Hypothermia ◽  
Vascular Protection ◽  
Impact Acceleration ◽  
Cerebral Vascular

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.

scholarly journals Technical aspects of an impact acceleration traumatic brain injury rat model with potential suitability for both microdialysis and PtiO2 monitoring

2004 ◽  
Vol 140 (1-2) ◽  
pp. 23-28 ◽  
Author(s):  
Emilie Carré ◽  
Emmanuel Cantais ◽  
Olivier Darbin ◽  
Jean-Pierre Terrier ◽  
Michel Lonjon ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rat Model ◽  
Technical Aspects ◽  
Impact Acceleration

scholarly journals Reproducibility and Characterization of Head Kinematics During a Large Animal Acceleration Model of Traumatic Brain Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Andrew R. Mayer ◽  
Josef M. Ling ◽  
Andrew B. Dodd ◽  
Julie G. Rannou-Latella ◽  
David D. Stephenson ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Animal Models ◽  
Angular Velocity ◽  
Diffuse Axonal Injury ◽  
Impulsive Loading ◽  
Large Animal ◽  
Head Kinematics ◽  
Large Animal Models ◽  
Acceleration Model

Acceleration parameters have been utilized for the last six decades to investigate pathology in both human and animal models of traumatic brain injury (TBI), design safety equipment, and develop injury thresholds. Previous large animal models have quantified acceleration from impulsive loading forces (i.e., machine/object kinematics) rather than directly measuring head kinematics. No study has evaluated the reproducibility of head kinematics in large animal models. Nine (five males) sexually mature Yucatan swine were exposed to head rotation at a targeted peak angular velocity of 250 rad/s in the coronal plane. The results indicated that the measured peak angular velocity of the skull was 51% of the impulsive load, was experienced over 91% longer duration, and was multi- rather than uni-planar. These findings were replicated in a second experiment with a smaller cohort (N = 4). The reproducibility of skull kinematics data was mostly within acceptable ranges based on published industry standards, although the coefficients of variation (8.9% for peak angular velocity or 12.3% for duration) were higher than the impulsive loading parameters produced by the machine (1.1 vs. 2.5%, respectively). Immunohistochemical markers of diffuse axonal injury and blood–brain barrier breach were not associated with variation in either skull or machine kinematics, suggesting that the observed levels of variance in skull kinematics may not be biologically meaningful with the current sample sizes. The findings highlight the reproducibility of a large animal acceleration model of TBI and the importance of direct measurements of skull kinematics to determine the magnitude of angular velocity, refine injury criteria, and determine critical thresholds.

Secondary ischemia impairing the restoration of ion homeostasis following traumatic brain injury

2005 ◽  
Vol 103 (4) ◽  
pp. 707-714 ◽  
Author(s):  
Michael F. Stiefel ◽  
Yoshiyuki Tomita ◽  
Anthony Marmarou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Ion Homeostasis ◽  
Cell Swelling ◽  
Forebrain Ischemia ◽  
Content Type ◽  
Ischemia Group ◽  
Impact Acceleration ◽  
Secondary Ischemia ◽  
Fine Print

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.

Recovery of Water Maze Performance in Aged Versus Young Rats After Brain Injury With the Impact Acceleration Model

2000 ◽  
Vol 17 (12) ◽  
pp. 1141-1153 ◽  
Author(s):  
PETER H. MAUGHAN ◽  
KEVIN J. SCHOLTEN ◽  
RICHARD H. SCHMIDT
Keyword(s):  
Brain Injury ◽  
Water Maze ◽  
Maze Performance ◽  
Young Rats ◽  
Acceleration Model ◽  
Impact Acceleration ◽  
The Impact

Cognitive control constrains memory attributions

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Control

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.

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