Traumatic Brain Injury

2019 ◽  
pp. 503-525
Author(s):  
Irene Cristofori ◽  
Jordan Grafman
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Future Research ◽  
Important Health ◽  
Behavioral Treatments ◽  
Severe Tbi ◽  
External Forces

Traumatic brain injury (TBI) is an alteration in brain structure or function caused by external forces that result in vascular and axonal damage, edema, and neuronal cell death. This chapter examines the spectrum of TBI. TBI is a major cause of death and disability and, therefore, an important health and socioeconomic problem for societies. Individuals surviving a moderate to severe TBI frequently suffer from long-lasting cognitive deficits. Such deficits include different aspects of cognition, such as memory, attention, executive functions, social behavior, and awareness. Protective factors, well-detailed diagnostic criteria, and available pharmacological and behavioral treatments are described. Final considerations on current controversies, knowledge gaps, and future research targets are provided.

Challenges and Opportunities for Neuroimaging in Young Patients with Traumatic Brain Injury: a Coordinated Effort towards Advancing Discovery from the ENIGMA Pediatric Moderate/Severe TBI Group

2019 ◽  
Author(s):  
Emily L. Dennis ◽  
Karen Caeyenberghs ◽  
Robert F. Asarnow ◽  
Talin Babikian ◽  
Brenda Bartnik-Olson ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Meta Analysis ◽  
Young Patients ◽  
Future Research ◽  
Childhood And Adolescence ◽  
Developmental Issues ◽  
Challenges And Opportunities ◽  
Severe Tbi ◽  
Advance Research

Traumatic brain injury (TBI) is a major cause of death and disability in children in both developed and developing nations. Children and adolescents suffer from TBI at a higher rate than the general population; however, research in this population lags behind research in adults. This may be due, in part, to the smaller number of investigators engaged in research with this population and may also be related to changes in safety laws and clinical practice that have altered length of hospital stays, treatment, and access to this population. Specific developmental issues also warrant attention in studies of children, and the ever-changing context of childhood and adolescence may require larger sample sizes than are commonly available to adequately address remaining questions related to TBI. The ENIGMA (Enhancing NeuroImaging Genetics through Meta-Analysis) Pediatric Moderate-Severe TBI (msTBI) group aims to advance research in this area through global collaborative meta-analysis. In this paper we discuss important challenges in pediatric TBI research and opportunities that we believe the ENIGMA Pediatric msTBI group can provide to address them. We conclude with recommendations for future research in this field of study.

Oxidative Stress: Major Threat in Traumatic Brain Injury

2018 ◽  
Vol 17 (9) ◽  
pp. 689-695 ◽  
Author(s):  
Nidhi Khatri ◽  
Manisha Thakur ◽  
Vikas Pareek ◽  
Sandeep Kumar ◽  
Sunil Sharma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mitochondrial Dysfunction ◽  
Calcium Influx ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Physical Assault ◽  
Mortality And Morbidity ◽  
Primary Injury

Background & Objective: Traumatic Brain Injury (TBI) is one of the major causes of mortality and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed by secondary injury which leads to biochemical, cellular, and physiological changes like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately people start facing some serious disabilies. Conclusion: In the present review we provide extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI.

Predictors of Emotional Distress in Family Caregivers of Persons with Traumatic Brain Injury: A Systematic Review

2013 ◽  
Vol 14 (1) ◽  
pp. 113-129 ◽  
Author(s):  
Angelle M. Sander ◽  
Kacey Little Maestas ◽  
Allison N. Clark ◽  
Whitney N. Havins
Keyword(s):  
Systematic Review ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Family Caregivers ◽  
Emotional Distress ◽  
Future Research ◽  
Class Iii ◽  
Class B ◽  
Assessment And Treatment ◽  
Severe Tbi

The purpose of the current paper was to conduct a systematic review of the literature on predictors of emotional distress in caregivers of persons with traumatic brain injury (TBI), and to provide evidence-based classification for prognostic variables to guide future research and clinical practice. A search was conducted using PubMed, CINAHL and PsycINFO databases. The citations of resulting articles were also reviewed. Twenty-eight articles met inclusion criteria and were retained for review. Reviews were conducted in accordance with the 2011 edition of the American Academy of Neurology (AAN) Guidelines for classifying evidence for prognostic studies. Data abstraction revealed one Class I study, four Class II studies, eight Class III studies, and 15 Class IV studies. Results of the review indicated that caregivers’ report of neurobehavioural problems in the person with injury is a probable predictor of emotional distress for caregivers of persons with complicated mild, moderate or severe TBI (Class B evidence). The level of participation in the person with injury, level of support needed by the person with injury, and family systems functioning are probably predictors of emotional distress for caregivers of persons with severe TBI (Class B evidence). Executive functioning impairment in the person with injury, pre-injury emotional distress in caregivers, caregiver age, caregivers’ use of emotion-focused coping, and social support may possibly be risk factors for caregivers’ emotional distress (Class C evidence). Recommendations for future research and implications for assessment and treatment of family caregivers are discussed.

scholarly journals Effects of Transient Receptor Potential Cation 5 (TRPC5) Inhibitor, NU6027, on Hippocampal Neuronal Death after Traumatic Brain Injury

2020 ◽  
Vol 21 (21) ◽  
pp. 8256 ◽  
Author(s):  
Min Kyu Park ◽  
Bo Young Choi ◽  
A Ra Kho ◽  
Song Hee Lee ◽  
Dae Ki Hong ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Death ◽  
Transient Receptor Potential ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Treated Group ◽  
Therapeutic Window ◽  
Permanent Disability ◽  
Fluoro Jade B

Traumatic brain injury (TBI) can cause physical, cognitive, social, and behavioral changes that can lead to permanent disability or death. After primary brain injury, translocated free zinc can accumulate in neurons and lead to secondary events such as oxidative stress, inflammation, edema, swelling, and cognitive impairment. Under pathological conditions, such as ischemia and TBI, excessive zinc release, and accumulation occurs in neurons. Based on previous research, it hypothesized that calcium as well as zinc would be influx into the TRPC5 channel. Therefore, we hypothesized that the suppression of TRPC5 would prevent neuronal cell death by reducing the influx of zinc and calcium. To test our hypothesis, we used a TBI animal model. After the TBI, we immediately injected NU6027 (1 mg/kg, intraperitoneal), TRPC5 inhibitor, and then sacrificed animals 24 h later. We conducted Fluoro-Jade B (FJB) staining to confirm the presence of degenerating neurons in the hippocampal cornus ammonis 3 (CA3). After the TBI, the degenerating neuronal cell count was decreased in the NU6027-treated group compared with the vehicle-treated group. Our findings suggest that the suppression of TRPC5 can open a new therapeutic window for a reduction of the neuronal death that may occur after TBI.

scholarly journals Safety and Efficacy of Erythropoietin in Traumatic Brain Injury Patients: A Pilot Randomized Trial

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
R. Nirula ◽  
R. Diaz-Arrastia ◽  
K. Brasel ◽  
J. A. Weigelt ◽  
K. Waxman
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Randomized Trial ◽  
Treatment Effect ◽  
Neuronal Cell Death ◽  
Neuron Specific Enolase ◽  
Neuronal Cell ◽  
Trauma Patients ◽  
Stroke Patients ◽  
Rule Out

Background. Erythropoietin (EPO) is a neuroprotective agent utilized in stroke patients. This pilot study represents the first randomized trial of EPO in traumatic brain injury (TBI) patients.Methods. Adult, blunt trauma patients with evidence of TBI were randomized to EPO or placebo within 6 hours of injury. Baseline and daily serum S-100B and Neuron Specific Enolase (NSE) levels were measured.Results. TBI was worse in the EPO (n=11) group compared to placebo patients (n=5). The use of EPO did not impact NSE (P=.89) or S100 B (P=.53) levels compared to placebo.Conclusions. At the dose used, EPO did not reduce neuronal cell death compared to placebo; however, TBI severity was worse in the EPO group while levels of NSE and S100-B were similar to the less injured placebo group making it difficult to rule out a treatment effect. A larger, balanced study is necessary to confirm a potential treatment effect.

scholarly journals Peroxisome Proliferator-Activated Receptors: “Key” Regulators of Neuroinflammation after Traumatic Brain Injury

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Philip F. Stahel ◽  
Wade R. Smith ◽  
Jay Bruchis ◽  
Craig H. Rabb
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Cell Death ◽  
Synthetic Cannabinoids ◽  
Experimental Studies ◽  
Neuronal Cell ◽  
Peroxisome Proliferator ◽  
Therapeutic Concept ◽  
Anti Inflammatory ◽  
Peroxisome Proliferator Activated Receptors

Traumatic brain injury is characterized by neuroinflammatory pathological sequelae which contribute to brain edema and delayed neuronal cell death. Until present, no specific pharmacological compound has been found, which attenuates these pathophysiological events and improves the outcome after head injury. Recent experimental studies suggest that targeting peroxisome proliferator-activated receptors (PPARs) may represent a new anti-inflammatory therapeutic concept for traumatic brain injury. PPARs are “key” transcription factors which inhibit NFκBactivity and downstream transcription products, such as proinflammatory and proapoptotic cytokines. The present review outlines our current understanding of PPAR-mediated neuroprotective mechanisms in the injured brain and discusses potential future anti-inflammatory strategies for head-injured patients, with an emphasis on the putative beneficial combination therapy of synthetic cannabinoids (e.g., dexanabinol) with PPARαagonists (e.g., fenofibrate).

scholarly journals Disruption of Bax Protein Prevents Neuronal Cell Death but Produces Cognitive Impairment in Mice following Traumatic Brain Injury

2008 ◽  
Vol 25 (7) ◽  
pp. 755-767 ◽  
Author(s):  
Roya Tehranian ◽  
Marie E. Rose ◽  
Vincent Vagni ◽  
Alicia M. Pickrell ◽  
Raymond P. Griffith ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Death ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Bax Protein

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.

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