Time Window for Voluntary Exercise–Induced Increases in Hippocampal Neuroplasticity Molecules after Traumatic Brain Injury Is Severity Dependent

2007 ◽  
Vol 24 (7) ◽  
pp. 1161-1171 ◽  
Author(s):  
Grace S. Griesbach ◽  
Fernando Gómez-Pinilla ◽  
David A. Hovda
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Time Window ◽  
Voluntary Exercise ◽  
Exercise Induced

scholarly journals Pterins as Diagnostic Markers of Mechanical and Impact-Induced Trauma: A Systematic Review

2019 ◽  
Vol 8 (9) ◽  
pp. 1383 ◽  
Author(s):  
Angus Lindsay ◽  
Gregory Baxter-Parker ◽  
Steven P. Gieseg
Keyword(s):  
Systematic Review ◽  
Traumatic Brain Injury ◽  
Cardiac Surgery ◽  
Brain Injury ◽  
Liver Resection ◽  
Review Of The Literature ◽  
Multiple Forms ◽  
Concentration Changes ◽  
Exercise Induced

We performed a systematic review of the literature to evaluate pterins as biomarkers of mechanical and impact-induced trauma. MEDLINE and Scopus were searched in March 2019. We included in vivo human studies that measured a pterin in response to mechanical or impact-induced trauma with no underlying prior disease or complication. We included 40 studies with a total of 3829 subjects. Seventy-seven percent of studies measured a significant increase in a pterin, primarily neopterin or total neopterin (neopterin + 7,8-dihydroneopterin). Fifty-one percent of studies measured an increase within 24 h or trauma, while 46% measured increases beyond 48 h. Pterins also showed promise as predictors of post-trauma complications such as sepsis, multi-organ failure and mortality. Exercise-induced trauma and traumatic brain injury caused an immediate increase in neopterin or total neopterin, while patients of multiple trauma had elevated pterin levels that remained above baseline for several days. Pterin concentration changes in response to surgery were variable with patients undergoing cardiac surgery having immediate and sustained pterin increases, while hysterectomy, liver resection or hysterectomy showed no change. This review provides systematic evidence that pterins, in particular neopterin and total neopterin, increase in response to multiple forms of mechanical or impact-induced trauma.

scholarly journals Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Kazuyuki Miyamoto ◽  
Hirokazu Ohtaki ◽  
Kenji Dohi ◽  
Tomomi Tsumuraya ◽  
Dandan Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Death ◽  
Time Window ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Therapeutic Time Window

Traumatic brain injury (TBI) is a major cause of death and disability in young people. No effective therapy is available to ameliorate its damaging effects. Our aim was to investigate the optimal therapeutic time window of edaravone, a free radical scavenger which is currently used in Japan. We also determined the temporal profile of reactive oxygen species (ROS) production, oxidative stress, and neuronal death. Male C57Bl/6 mice were subjected to a controlled cortical impact (CCI). Edaravone (3.0 mg/kg), or vehicle, was administered intravenously at 0, 3, or 6 hours following CCI. The production of superoxide radicals (O2∙-) as a marker of ROS, of nitrotyrosine (NT) as an indicator of oxidative stress, and neuronal death were measured for 24 hours following CCI. Superoxide radical production was clearly evident 3 hours after CCI, with oxidative stress and neuronal cell death becoming apparent after 6 hours. Edaravone administration after CCI resulted in a significant reduction in the injury volume and oxidative stress, particularly at the 3-hour time point. Moreover, the greatest decrease inO2∙-levels was observed when edaravone was administered 3 hours following CCI. These findings suggest that edaravone could prove clinically useful to ameliorate the devastating effects of TBI.

scholarly journals Effects of concussion on the blood–brain barrier in humans and rodents

2017 ◽  
Vol 1 ◽  
pp. 205970021668451 ◽  
Author(s):  
Ronald Sahyouni ◽  
Paula Gutierrez ◽  
Eric Gold ◽  
Richard T Robertson ◽  
Brian J Cummings
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Blood Brain Barrier ◽  
Time Course ◽  
Time Window ◽  
The United States ◽  
Model Systems ◽  
Brain Barrier ◽  
Tracer Injection ◽  
Blood Brain

Traumatic brain injury and the long-term consequences of repeated concussions constitute mounting concerns in the United States, with 5.3 million individuals living with a traumatic brain injury-related disability. Attempts to understand mechanisms and possible therapeutic approaches to alleviate the consequences of repeat mild concussions or traumatic brain injury on cerebral vasculature depend on several aspects of the trauma, including: (1) the physical characteristics of trauma or insult that result in damage; (2) the time “window” after trauma in which neuropathological features develop; (3) methods to detect possible breakdown of the blood–brain barrier; and (4) understanding different consequences of a single concussion as compared with multiple concussions. We review the literature to summarize the current understanding of blood–brain barrier and endothelial cell changes post-neurotrauma in concussions and mild traumatic brain injury. Attention is focused on concussion and traumatic brain injury in humans, with a goal of pointing out the gaps in our knowledge and how studies of rodent model systems of concussion may help in filling these gaps. Specifically, we focus on disruptions that concussion causes to the blood–brain barrier and its multifaceted consequences. Importantly, the magnitude of post-concussion blood–brain barrier dysfunction may influence the time course and extent of neuronal recovery; hence, we include in this review comparisons of more severe traumatic brain injury to concussion where appropriate. Finally, we address the important, and still unresolved, issue of how best to detect possible breakdown in the blood–brain barrier following neurotrauma by exploring intravascular tracer injection in animal models to examine leakage into the brain parenchyma.

Establishment of an ideal time window model in hypothermic-targeted temperature management after traumatic brain injury in rats

2017 ◽  
Vol 1669 ◽  
pp. 141-149 ◽  
Author(s):  
Wan-Yong Zhao ◽  
Shao-Bo Chen ◽  
Jing-Jing Wang ◽  
Chao Xu ◽  
Ming-Liang Zhao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Time Window ◽  
Targeted Temperature Management ◽  
Temperature Management

scholarly journals One-Year Prospective Study of Plasma Biomarkers From CNS in Patients With Mild Traumatic Brain Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Gerard Janez Brett Clarke ◽  
Toril Skandsen ◽  
Henrik Zetterberg ◽  
Cathrine Elisabeth Einarsen ◽  
Casper Feyling ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glial Fibrillary Acidic Protein ◽  
Mild Traumatic Brain Injury ◽  
Time Window ◽  
Brain Mri ◽  
Demographic Variables ◽  
Acidic Protein ◽  
Observation Study ◽  
Diagnostic Time

Objective: To investigate the longitudinal evolution of three blood biomarkers: neurofilament light (NFL), glial fibrillary acidic protein (GFAP) and tau, in out-patients and hospitalized patients with mild traumatic brain injury (mTBI) compared to controls, along with their associations—in patients—with clinical injury characteristics and demographic variables, and ability to discriminate patients with mTBI from controls.Methods: A longitudinal observation study including 207 patients with mTBI, 84 age and sex-matched community controls (CCs) and 52 trauma controls (TCs). Blood samples were collected at 5 timepoints: acute (<24 h), 72 h (24–72 h post-injury), 2 weeks, 3 and 12 months. Injury-related, clinical and demographic variables were obtained at inclusion and brain MRI within 72 h.Results: Plasma GFAP and tau were most elevated acutely and NFL at 2 weeks and 3 months. The group of patients with mTBI and concurrent other somatic injuries (mTBI+) had the highest elevation in all biomarkers across time points, and were more likely to be victims of traffic accidents and violence. All biomarkers were positively associated with traumatic intracranial findings on MRI obtained within 72 h. Glial fibrillary acidic protein and NFL levels were associated with Glasgow Coma Scale (GCS) score and presence of other somatic injuries. Acute GFAP concentrations showed the highest discriminability between patients and controls with an Area Under the Curve (AUC) of 0.92. Acute tau and 2-week NFL concentrations showed moderate discriminability (AUC = 0.70 and AUC = 0.75, respectively). Tau showed high discriminability between mTBI+ and TCs (AUC = 0.80).Conclusions: The association of plasma NFL with traumatic intracranial MRI findings, together with its later peak, could reflect ongoing secondary injury or repair mechanisms, allowing for a protracted diagnostic time window. Patients experiencing both mTBI and other injuries appear to be a subgroup with greater neural injury, differing from both the mTBI without other injuries and from both control groups. Acute GFAP concentrations showed the highest discriminability between patients and controls, were highly associated with intracranial traumatic injury, and showed the largest elevations compared to controls at the acute timepoint, suggesting it to be the most clinically useful plasma biomarker of primary CNS injury in mTBI.

scholarly journals Interactions among Genetic Background, Anesthetic Agent, and Oxygen Concentration Shape Blunt Traumatic Brain Injury Outcomes in Drosophila melanogaster

2020 ◽  
Vol 21 (18) ◽  
pp. 6926
Author(s):  
Amanda R. Scharenbrock ◽  
Hannah J. Schiffman ◽  
Zachariah P. G. Olufs ◽  
David A. Wassarman ◽  
Misha Perouansky
Keyword(s):  
Traumatic Brain Injury ◽  
Drosophila Melanogaster ◽  
Brain Injury ◽  
Genetic Background ◽  
Time Window ◽  
Fruit Fly ◽  
Therapeutic Interventions ◽  
General Anesthetics ◽  
Secondary Injuries ◽  
Locomotor Impairment

Following traumatic brain injury (TBI), the time window during which secondary injuries develop provides a window for therapeutic interventions. During this time, many TBI victims undergo exposure to hyperoxia and anesthetics. We investigated the effects of genetic background on the interaction of oxygen and volatile general anesthetics with brain pathophysiology after closed-head TBI in the fruit fly Drosophila melanogaster. To test whether sevoflurane shares genetic risk factors for mortality with isoflurane and whether locomotion is affected similarly to mortality, we used a device that generates acceleration–deceleration forces to induce TBI in ten inbred fly lines. After TBI, we exposed flies to hyperoxia alone or in combination with isoflurane or sevoflurane and quantified mortality and locomotion 24 and 48 h after TBI. Modulation of TBI–induced mortality and locomotor impairment by hyperoxia with or without anesthetics varied among fly strains and among combinations of agents. Resistance to increased mortality from hyperoxic isoflurane predicted resistance to increased mortality from hyperoxic sevoflurane but did not predict the degree of locomotion impairment under any condition. These findings are important because they demonstrate that, in the context of TBI, genetic background determines the latent toxic potentials of oxygen and anesthetics.

Sign in / Sign up

Export Citation Format

Share Document