Age-dependent reduction of cortical contusion volume by ketones after traumatic brain injury

2005 ◽  
Vol 82 (3) ◽  
pp. 413-420 ◽  
Author(s):  
M.L. Prins ◽  
L.S. Fujima ◽  
D.A. Hovda
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Age Dependent ◽  
Cortical Contusion

scholarly journals Divergent age-dependent peripheral immune transcriptomic profile following traumatic brain injury

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Amanda Hazy ◽  
Lauren Bochicchio ◽  
Andrea Oliver ◽  
Eric Xie ◽  
Shuo Geng ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Transcriptomic Profile ◽  
Age Dependent

scholarly journals A combination antioxidant therapy to inhibit NOX2 and activate Nrf2 decreases secondary brain damage and improves functional recovery after traumatic brain injury

2017 ◽  
Vol 38 (10) ◽  
pp. 1818-1827 ◽  
Author(s):  
Raghavendar Chandran ◽  
TaeHee Kim ◽  
Suresh L Mehta ◽  
Eshwar Udho ◽  
Vishal Chanana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Motor Function ◽  
Neurological Dysfunction ◽  
Vehicle Group ◽  
Lesion Volume ◽  
Post Injury ◽  
Cortical Contusion ◽  
Nrf2 Activator

Uncontrolled oxidative stress contributes to the secondary neuronal death that promotes long-term neurological dysfunction following traumatic brain injury (TBI). Surprisingly, both NADPH oxidase 2 (NOX2) that increases and transcription factor Nrf2 that decreases reactive oxygen species (ROS) are induced after TBI. As the post-injury functional outcome depends on the balance of these opposing molecular pathways, we evaluated the effect of TBI on the motor and cognitive deficits and cortical contusion volume in NOX2 and Nrf2 knockout mice. Genetic deletion of NOX2 improved, while Nrf2 worsened the post-TBI motor function recovery and lesion volume indicating that decreasing ROS levels might be beneficial after TBI. Treatment with either apocynin (NOX2 inhibitor) or TBHQ (Nrf2 activator) alone significantly improved the motor function after TBI, but had no effect on the lesion volume, compared to vehicle control. Whereas, the combo therapy (apocynin + TBHQ) given at either 5 min/24 h or 2 h/24 h improved motor and cognitive function and decreased cortical contusion volume compared to vehicle group. Thus, both the generation and disposal of ROS are important modulators of oxidative stress, and a combo therapy that prevents ROS formation and potentiates ROS disposal concurrently is efficacious after TBI.

Age-Dependent Effects of Severe Traumatic Brain Injury on Cerebral Dopaminergic Activity in Newborn and Juvenile Pigs

2004 ◽  
Vol 21 (8) ◽  
pp. 1076-1089 ◽  
Author(s):  
Bernd Walter ◽  
Peter Brust ◽  
Frank Füchtner ◽  
Marco Müller ◽  
Rainer Hinz ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Dopaminergic Activity ◽  
Age Dependent

scholarly journals Age-dependent release of high-mobility group box protein-1 and cellular neuroinflammation after traumatic brain injury in mice

2018 ◽  
Vol 527 (6) ◽  
pp. 1102-1117 ◽  
Author(s):  
Kyria M. Webster ◽  
Mujun Sun ◽  
Peter J. Crack ◽  
Terence J. O'Brien ◽  
Sandy R. Shultz ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
High Mobility ◽  
High Mobility Group ◽  
Age Dependent

scholarly journals Hyperostosis Frontalis Interna in a Child With Severe Traumatic Brain Injury

2017 ◽  
Vol 4 ◽  
pp. 2329048X1770055
Author(s):  
Yaxiong Li ◽  
Xin Wang ◽  
Yan Li
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Clinical Case ◽  
Frontal Bone ◽  
Related Literature ◽  
The Past ◽  
Age Dependent

Hyperostosis frontalis interna is an unexplained irregular thickening of the inner table of the frontal bone. Hyperostosis frontalis interna was first identified in 1719 by Morgagni as a symptom of a more generalized syndrome characterized by virilism and obesity. Most current studies have shown hyperostosis frontalis interna to be a sex- and age-dependent phenomenon, and females manifest a significantly higher prevalence of hyperostosis frontalis interna than males. In this article, the authors report the clinical case of hyperostosis frontalis interna in a 7-year-old child who had severe traumatic brain injury in the past; review the related literature; and discuss the clinical, radiological, and therapeutic features of this condition.

Stilbazulenyl nitrone, a novel azulenyl nitrone antioxidant, improved neurological deficit and reduced contusion size after traumatic brain injury in rats

2002 ◽  
Vol 96 (6) ◽  
pp. 1077-1083 ◽  
Author(s):  
Ludmila Belayev ◽  
David A. Becker ◽  
Ofelia F. Alonso ◽  
Yitao Liu ◽  
Raul Busto ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Temperature ◽  
Antioxidant Properties ◽  
Neurological Status ◽  
Sprague Dawley ◽  
Content Type ◽  
Fluid Percussion ◽  
Cortical Contusion ◽  
Fine Print

Object. Stilbazulenyl nitrone (STAZN) is a second-generation azulenyl nitrone that has markedly enhanced antioxidant properties compared with those of conventional alpha-phenyl nitrones. In this study, the authors assessed the potential efficacy of STAZN in a rodent model of fluid-percussion brain injury, which results in a consistent cortical contusion. Methods. After anesthesia had been induced in normothermic Sprague—Dawley rats (brain temperature 36–36.5°C) by halothane—nitrous oxide, the animals were subjected to a right parietooccipital parasagittal fluid-percussion injury (1.5–2 atm). The agent (STAZN, 30 mg/kg; eight animals) or vehicle (dimethyl sulfoxide; eight animals) was administered intraperitoneally at 5 minutes and 4 hours after trauma. The neurological status of each rat was evaluated on Days 1, 2, and 7 postinjury (normal score 0, maximum injury 12). Seven days after trauma, the rat brains were perfusion fixed, coronal sections at various levels were digitized, and areas of contusion were measured. Treatment with STAZN significantly improved neurological scores on Days 2 and 7 postinjury compared with vehicle-treated rats. Administration of STAZN also significantly reduced the total contusion area by 63% (1.8 ± 0.5 mm2 in STAZN-treated animals compared with 4.8 ± 2.1 mm2 in vehicle-treated animals; p = 0.04) and the deep cortical contusion area by 60% (1.2 ± 0.2 mm2 in STAZN-treated animals compared with 2.9 ± 1.2 mm2 in vehicle-treated animals; p = 0.03). By contrast, hippocampal cell loss in the CA3 sector was unaffected by STAZN treatment. Conclusions. Therapy with STAZN, a novel potent antioxidant, administered following traumatic brain injury, markedly improves neurological and histological outcomes. Azulenyl nitrones appear to represent a promising class of neuroprotective agents for combating this devastating condition.

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