Science.gov

Sample records for abstract traumatic brain

  1. Abstracting meaning from complex information (gist reasoning) in adult traumatic brain injury.

    PubMed

    Vas, Asha Kuppachi; Spence, Jeffrey; Chapman, Sandra Bond

    2015-01-01

    Gist reasoning (abstracting meaning from complex information) was compared between adults with moderate-to-severe traumatic brain injury (TBI, n = 30) at least one year post injury and healthy adults (n = 40). The study also examined the contribution of executive functions (working memory, inhibition, and switching) and memory (immediate recall and memory for facts) to gist reasoning. The correspondence between gist reasoning and daily function was also examined in the TBI group. Results indicated that the TBI group performed significantly lower than the control group on gist reasoning, even after adjusting for executive functions and memory. Executive function composite was positively associated with gist reasoning (p < .001). Additionally, performance on gist reasoning significantly predicted daily function in the TBI group beyond the predictive ability of executive function alone (p = .011). Synthesizing and abstracting meaning(s) from information (i.e., gist reasoning) could provide an informative index into higher order cognition and daily functionality. PMID:25633568

  2. Traumatic Brain Injury

    MedlinePlus

    ... Center PTACs Workspaces Log-in Search for: Traumatic Brain Injury A legacy resource from NICHCY Disability Fact ... in her. Back to top What is Traumatic Brain Injury? A traumatic brain injury (TBI) is an ...

  3. Traumatic Brain Injury

    MedlinePlus

    Traumatic brain injury (TBI) happens when a bump, blow, jolt, or other head injury causes damage to the brain. Every year, millions of people in the U.S. suffer brain injuries. More than half are bad enough that ...

  4. Experimental traumatic brain injury

    PubMed Central

    2010-01-01

    Traumatic brain injury, a leading cause of death and disability, is a result of an outside force causing mechanical disruption of brain tissue and delayed pathogenic events which collectively exacerbate the injury. These pathogenic injury processes are poorly understood and accordingly no effective neuroprotective treatment is available so far. Experimental models are essential for further clarification of the highly complex pathology of traumatic brain injury towards the development of novel treatments. Among the rodent models of traumatic brain injury the most commonly used are the weight-drop, the fluid percussion, and the cortical contusion injury models. As the entire spectrum of events that might occur in traumatic brain injury cannot be covered by one single rodent model, the design and choice of a specific model represents a major challenge for neuroscientists. This review summarizes and evaluates the strengths and weaknesses of the currently available rodent models for traumatic brain injury. PMID:20707892

  5. Traumatic Brain Injury

    MedlinePlus

    ... disabilities include problems with cognition (thinking, memory, and reasoning), sensory processing (sight, hearing, touch, taste, and smell), ... barrier. NIH Patient Recruitment for Traumatic Brain Injury Clinical Trials At NIH Clinical Center Throughout the U.S. ...

  6. Traumatic Brain Injury

    MedlinePlus

    ... a concussion may feel dazed and may lose vision or balance for a while after the injury A brain contusion is a bruise of the brain. This ... consciousness Headache Confusion Feeling dizzy or lightheaded Blurry vision ... or severe traumatic brain injury include all of the symptoms listed above ...

  7. Pediatric Traumatic Brain Injury.

    PubMed

    Schaller, Alexandra L; Lakhani, Saquib A; Hsu, Benson S

    2015-10-01

    The purpose of this article is to provide a better understanding of pediatric traumatic brain injury and its management. Within the pediatric age group, ages 1 to 19, injuries are the number one cause of death with traumatic brain injury being involved in almost 50 percent of these cases. This, along with the fact that the medical system spends over $1 billion annually on pediatric traumatic brain injury, makes this issue both timely and relevant to health care providers. Over the course of this article the epidemiology, physiology, pathophysiology, and treatment of pediatric traumatic brain injury will be explored. Emphasis will be placed on the role of the early responder and the immediate interventions that should be considered and/or performed. The management discussed in this article follows the most recent recommendations from the 2012 edition of the Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents. Despite the focus of this article, it is important not to lose sight of the fact that an ounce of prevention is worth a pound--or, to be more precise and use the average human's brain measurements, just above three pounds--of cure. PMID:26630835

  8. [Traumatic brain injury].

    PubMed

    Hackenberg, K; Unterberg, A

    2016-02-01

    Since traumatic brain injury is the most common cause of long-term disability and death among young adults, it represents an enormous socio-economic and healthcare burden. As a consequence of the primary lesion, a perifocal brain edema develops causing an elevation of the intracranial pressure due to the limited intracranial space. This entails a reduction of the cerebral perfusion pressure and the cerebral blood flow. A cerebral perfusion deficit below the threshold for ischemia leads to further ischemic lesions and to a progression of the contusion. As the irreversible primary lesion can only be inhibited by primary prevention, the therapy of traumatic brain injury focuses on the secondary injuries. The treatment consists of surgical therapy evacuating the space-occupying intracranial lesion and conservative intensive medical care. Due to the complex pathophysiology the therapy of traumatic brain injury should be rapidly performed in a neurosurgical unit. PMID:26810405

  9. Traumatic Brain Injury (TBI)

    MedlinePlus

    ... A. (2008). Mild traumatic brain injury in U.S. soldiers returning from Iraq. New England Journal of Medicine, 358, 453–463. ... and Spotlights U.S. hospitals miss followup for suspected child abuse Q&A with NICHD Acting Director Catherine ...

  10. Traumatic brain injury

    PubMed Central

    Risdall, Jane E.; Menon, David K.

    2011-01-01

    There is an increasing incidence of military traumatic brain injury (TBI), and similar injuries are seen in civilians in war zones or terrorist incidents. Indeed, blast-induced mild TBI has been referred to as the signature injury of the conflicts in Iraq and Afghanistan. Assessment involves schemes that are common in civilcian practice but, in common with civilian TBI, takes little account of information available from modern imaging (particularly diffusion tensor magnetic resonance imaging) and emerging biomarkers. The efficient logistics of clinical care delivery in the field may have a role in optimizing outcome. Clinical care has much in common with civilian TBI, but intracranial pressure monitoring is not always available, and protocols need to be modified to take account of this. In addition, severe early oedema has led to increasing use of decompressive craniectomy, and blast TBI may be associated with a higher incidence of vasospasm and pseudoaneurysm formation. Visual and/or auditory deficits are common, and there is a significant risk of post-traumatic epilepsy. TBI is rarely an isolated finding in this setting, and persistent post-concussive symptoms are commonly associated with post-traumatic stress disorder and chronic pain, a constellation of findings that has been called the polytrauma clinical triad. PMID:21149359

  11. Mild traumatic brain injury.

    PubMed

    Katz, Douglas I; Cohen, Sara I; Alexander, Michael P

    2015-01-01

    Mild traumatic brain injury (TBI) is common but accurate diagnosis and defining criteria for mild TBI and its clinical consequences have been problematic. Mild TBI causes transient neurophysiologic brain dysfunction, sometimes with structural axonal and neuronal damage. Biomarkers, such as newer imaging technologies and protein markers, are promising indicators of brain injury but are not ready for clinical use. Diagnosis relies on clinical criteria regarding depth and duration of impaired consciousness and amnesia. These criteria are particularly difficult to confirm at the least severe end of the mild TBI continuum, especially when relying on subjective, retrospective accounts. The postconcussive syndrome is a controversial concept because of varying criteria, inconsistent symptom clusters and the evidence that similar symptom profiles occur with other disorders, and even in a proportion of healthy individuals. The clinical consequences of mild TBI can be conceptualized as two multidimensional disorders: (1) a constellation of acute symptoms that might be termed early phase post-traumatic disorder (e.g., headache, dizziness, imbalance, fatigue, sleep disruption, impaired cognition), that typically resolve in days to weeks and are largely related to brain trauma and concomitant injuries; (2) a later set of symptoms, a late phase post-traumatic disorder, evolving out of the early phase in a minority of patients, with a more prolonged (months to years), sometimes worsening set of somatic, emotional, and cognitive symptoms. The later phase disorder is highly influenced by a variety of psychosocial factors and has little specificity for brain injury, although a history of multiple concussions seems to increase the risk of more severe and longer duration symptoms. Effective early phase management may prevent or limit the later phase disorder and should include education about symptoms and expectations for recovery, as well as recommendations for activity modifications

  12. Traumatic Alterations in Consciousness: Traumatic Brain Injury

    PubMed Central

    Blyth, Brian J.; Bazarian, Jeffrey J.

    2010-01-01

    Mild traumatic brain injury (mTBI) refers to the clinical condition of transient alteration of consciousness as a result of traumatic injury to the brain. The priority of emergency care is to identify and facilitate the treatment of rare but potentially life threatening intra-cranial injuries associated with mTBI through the judicious application of appropriate imaging studies and neurosurgical consultation. Although post-mTBI symptoms quickly and completely resolve in the vast majority of cases, a significant number of patients will complain of lasting problems that may cause significant disability. Simple and early interventions such as patient education and appropriate referral can reduce the likelihood of chronic symptoms. Although definitive evidence is lacking, mTBI is likely to be related to significant long-term sequelae such as Alzheimer's disease and other neurodegenerative processes. PMID:20709244

  13. Traumatic Brain Injury Inpatient Rehabilitation

    ERIC Educational Resources Information Center

    Im, Brian; Schrer, Marcia J.; Gaeta, Raphael; Elias, Eileen

    2010-01-01

    Traumatic brain injuries (TBI) can cause multiple medical and functional problems. As the brain is involved in regulating nearly every bodily function, a TBI can affect any part of the body and aspect of cognitive, behavioral, and physical functioning. However, TBI affects each individual differently. Optimal management requires understanding the…

  14. Traumatic Brain Injury: FDA Research and Actions

    MedlinePlus

    ... For Consumers Home For Consumers Consumer Updates Traumatic Brain Injury: FDA Research and Actions Share Tweet Linkedin ... top What to Do if You Suspect Traumatic Brain Injury Anyone with signs of moderate or severe ...

  15. Knowledge of Traumatic Brain Injury among Educators

    ERIC Educational Resources Information Center

    Ernst, William J.; Gallo, Adrienne B.; Sellers, Amanda L.; Mulrine, Jessica; MacNamara, Luciana; Abrahamson, Allison; Kneavel, Meredith

    2016-01-01

    The purpose of this study is to determine knowledge of traumatic brain injury among educators. Few studies have examined knowledge of traumatic brain injury in this population and fewer still have included a substantial proportion of general education teachers. Examining knowledge of traumatic brain injury in educators is important as the vast…

  16. Evaluation after Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Trudel, Tina M.; Halper, James; Pines, Hayley; Cancro, Lorraine

    2010-01-01

    It is important to determine if a traumatic brain injury (TBI) has occurred when an individual is assessed in a hospital emergency room after a car accident, fall, or other injury that affects the head. This determination influences decisions about treatment. It is essential to screen for the injury, because the sooner they begin appropriate…

  17. Hypothermia in Traumatic Brain Injury.

    PubMed

    Ahmed, Aminul I; Bullock, M Ross; Dietrich, W Dalton

    2016-10-01

    For over 50 years, clinicians have used hypothermia to manage traumatic brain injury (TBI). In the last two decades numerous trials have assessed whether hypothermia is of benefit in patients. Mild to moderate hypothermia reduces the intracranial pressure (ICP). Randomized control trials for short-term hypothermia indicate no benefit in outcome after severe TBI, whereas longer-term hypothermia could be of benefit by reducing ICP. This article summarises current evidence and gives recommendations based upon the conclusions. PMID:27637398

  18. Chronic Traumatic Encephalopathy: The Neuropathological Legacy of Traumatic Brain Injury.

    PubMed

    Hay, Jennifer; Johnson, Victoria E; Smith, Douglas H; Stewart, William

    2016-05-23

    Almost a century ago, the first clinical account of the punch-drunk syndrome emerged, describing chronic neurological and neuropsychiatric sequelae occurring in former boxers. Thereafter, throughout the twentieth century, further reports added to our understanding of the neuropathological consequences of a career in boxing, leading to descriptions of a distinct neurodegenerative pathology, termed dementia pugilistica. During the past decade, growing recognition of this pathology in autopsy studies of nonboxers who were exposed to repetitive, mild traumatic brain injury, or to a single, moderate or severe traumatic brain injury, has led to an awareness that it is exposure to traumatic brain injury that carries with it a risk of this neurodegenerative disease, not the sport or the circumstance in which the injury is sustained. Furthermore, the neuropathology of the neurodegeneration that occurs after traumatic brain injury, now termed chronic traumatic encephalopathy, is acknowledged as being a complex, mixed, but distinctive pathology, the detail of which is reviewed in this article. PMID:26772317

  19. Pathophysiology of Traumatic Brain Injury.

    PubMed

    McGinn, Melissa J; Povlishock, John T

    2016-10-01

    This article provides a concise overview, at the structural and functional level, of those changes evoked by traumatic brain injury across the spectrum of the disease. Using data derived from animals and humans, the pathogenesis of focal versus diffuse brain damage is presented for consideration of its overall implications for morbidity. Emphasis is placed on contusion and its potential expansion in concert with diffuse changes primarily assessed at the axonal level. Concomitant involvement of neuroexcitation and its role in global and focal metabolic changes is considered. Lastly, the influence of premorbid factors including age, genetics, and socioeconomic background is discussed. PMID:27637392

  20. Imaging of Traumatic Brain Injury.

    PubMed

    Bodanapally, Uttam K; Sours, Chandler; Zhuo, Jiachen; Shanmuganathan, Kathirkamanathan

    2015-07-01

    Imaging plays an important role in the management of patients with traumatic brain injury (TBI). Computed tomography (CT) is the first-line imaging technique allowing rapid detection of primary structural brain lesions that require surgical intervention. CT also detects various deleterious secondary insults allowing early medical and surgical management. Serial imaging is critical to identifying secondary injuries. MR imaging is indicated in patients with acute TBI when CT fails to explain neurologic findings. However, MR imaging is superior in patients with subacute and chronic TBI and also predicts neurocognitive outcome.

  1. Traumatic brain injury and reserve.

    PubMed

    Bigler, Erin D; Stern, Yaakov

    2015-01-01

    The potential role of brain and cognitive reserve in traumatic brain injury (TBI) is reviewed. Brain reserve capacity (BRC) refers to preinjury quantitative measures such as brain size that relate to outcome. Higher BRC implies threshold differences when clinical deficits will become apparent after injury, where those individuals with higher BRC require more pathology to reach that threshold. Cognitive reserve (CR) refers to how flexibly and efficiently the individual makes use of available brain resources. The CR model suggests the brain actively attempts to cope with brain damage by using pre-existing cognitive processing approaches or by enlisting compensatory approaches. Standard proxies for CR include education and IQ although this has expanded to include literacy, occupational attainment, engagement in leisure activities, and the integrity of social networks. Most research on BRC and CR has taken place in aging and degenerative disease but these concepts likely apply to the effects of TBI, especially with regards to recovery. Since high rates of TBI occur in those under age 35, both CR and BRC factors likely relate to how the individual copes with TBI over the lifespan. These factors may be particularly relevant to the relationship of developing dementia in the individual who has sustained a TBI earlier in life.

  2. The neuropathology of traumatic brain injury.

    PubMed

    Mckee, Ann C; Daneshvar, Daniel H

    2015-01-01

    Traumatic brain injury, a leading cause of mortality and morbidity, is divided into three grades of severity: mild, moderate, and severe, based on the Glasgow Coma Scale, the loss of consciousness, and the development of post-traumatic amnesia. Although mild traumatic brain injury, including concussion and subconcussion, is by far the most common, it is also the most difficult to diagnose and the least well understood. Proper recognition, management, and treatment of acute concussion and mild traumatic brain injury are the fundamentals of an emerging clinical discipline. It is also becoming increasingly clear that some mild traumatic brain injuries have persistent, and sometimes progressive, long-term debilitating effects. Evidence indicates that a single traumatic brain injury can precipitate or accelerate multiple age-related neurodegenerations, increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease, and that repetitive mild traumatic brain injuries can provoke the development of a tauopathy, chronic traumatic encephalopathy. Clinically, chronic traumatic encephalopathy is associated with behavioral changes, executive dysfunction, memory loss, and cognitive impairments that begin insidiously and progress slowly over decades. Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus, septal abnormalities, and abnormal deposits of hyperphosphorylated tau (τ) as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy frequently occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including Alzheimer's disease, Lewy body disease, and motor neuron disease. Currently, chronic traumatic encephalopathy can be diagnosed only at

  3. Traumatic Brain Injury: A Challenge for Educators

    ERIC Educational Resources Information Center

    Bullock, Lyndal M.; Gable, Robert A.; Mohr, J. Darrell

    2005-01-01

    In this article, the authors provide information designed to enhance the knowledge and understanding of school personnel about traumatic brain injury (TBI). The authors specifically define TBI and enumerate common characteristics associated with traumatic brain injury, discuss briefly the growth and type of services provided, and offer some…

  4. Pathology of traumatic brain injury.

    PubMed

    Finnie, John W

    2014-12-01

    Although traumatic brain injury (TBI) is frequently encountered in veterinary practice in companion animals, livestock and horses, inflicted head injury is a common method of euthanasia in domestic livestock, and malicious head trauma can lead to forensic investigation, the pathology of TBI has generally received little attention in the veterinary literature. This review highlights the pathology and pathogenesis of cerebral lesions produced by blunt, non-missile and penetrating, missile head injuries as an aid to the more accurate diagnosis of neurotrauma cases. If more cases of TBI in animals that result in fatality or euthanasia are subjected to rigorous neuropathological examination, this will lead to a better understanding of the nature and development of brain lesions in these species, rather than extrapolating data from human studies. PMID:25178417

  5. Preconditioning for traumatic brain injury

    PubMed Central

    Yokobori, Shoji; Mazzeo, Anna T; Hosein, Khadil; Gajavelli, Shyam; Dietrich, W. Dalton; Bullock, M. Ross

    2016-01-01

    Traumatic brain injury (TBI) treatment is now focused on the prevention of primary injury and reduction of secondary injury. However, no single effective treatment is available as yet for the mitigation of traumatic brain damage in humans. Both chemical and environmental stresses applied before injury, have been shown to induce consequent protection against post-TBI neuronal death. This concept termed “preconditioning” is achieved by exposure to different pre-injury stressors, to achieve the induction of “tolerance” to the effect of the TBI. However, the precise mechanisms underlying this “tolerance” phenomenon are not fully understood in TBI, and therefore even less information is available about possible indications in clinical TBI patients. In this review we will summarize TBI pathophysiology, and discuss existing animal studies demonstrating the efficacy of preconditioning in diffuse and focal type of TBI. We will also review other non-TBI preconditionng studies, including ischemic, environmental, and chemical preconditioning, which maybe relevant to TBI. To date, no clinical studies exist in this field, and we speculate on possible futureclinical situation, in which pre-TBI preconditioning could be considered. PMID:24323189

  6. Traumatic brain injury-induced sleep disorders.

    PubMed

    Viola-Saltzman, Mari; Musleh, Camelia

    2016-01-01

    Sleep disturbances are frequently identified following traumatic brain injury, affecting 30%-70% of persons, and often occur after mild head injury. Insomnia, fatigue, and sleepiness are the most frequent sleep complaints after traumatic brain injury. Sleep apnea, narcolepsy, periodic limb movement disorder, and parasomnias may also occur after a head injury. In addition, depression, anxiety, and pain are common brain injury comorbidities with significant influence on sleep quality. Two types of traumatic brain injury that may negatively impact sleep are acceleration/deceleration injuries causing generalized brain damage and contact injuries causing focal brain damage. Polysomnography, multiple sleep latency testing, and/or actigraphy may be utilized to diagnose sleep disorders after a head injury. Depending on the disorder, treatment may include the use of medications, positive airway pressure, and/or behavioral modifications. Unfortunately, the treatment of sleep disorders associated with traumatic brain injury may not improve neuropsychological function or sleepiness. PMID:26929626

  7. Traumatic brain injury-induced sleep disorders

    PubMed Central

    Viola-Saltzman, Mari; Musleh, Camelia

    2016-01-01

    Sleep disturbances are frequently identified following traumatic brain injury, affecting 30%–70% of persons, and often occur after mild head injury. Insomnia, fatigue, and sleepiness are the most frequent sleep complaints after traumatic brain injury. Sleep apnea, narcolepsy, periodic limb movement disorder, and parasomnias may also occur after a head injury. In addition, depression, anxiety, and pain are common brain injury comorbidities with significant influence on sleep quality. Two types of traumatic brain injury that may negatively impact sleep are acceleration/deceleration injuries causing generalized brain damage and contact injuries causing focal brain damage. Polysomnography, multiple sleep latency testing, and/or actigraphy may be utilized to diagnose sleep disorders after a head injury. Depending on the disorder, treatment may include the use of medications, positive airway pressure, and/or behavioral modifications. Unfortunately, the treatment of sleep disorders associated with traumatic brain injury may not improve neuropsychological function or sleepiness. PMID:26929626

  8. Neurostimulation for traumatic brain injury.

    PubMed

    Shin, Samuel S; Dixon, C Edward; Okonkwo, David O; Richardson, R Mark

    2014-11-01

    Traumatic brain injury (TBI) remains a significant public health problem and is a leading cause of death and disability in many countries. Durable treatments for neurological function deficits following TBI have been elusive, as there are currently no FDA-approved therapeutic modalities for mitigating the consequences of TBI. Neurostimulation strategies using various forms of electrical stimulation have recently been applied to treat functional deficits in animal models and clinical stroke trials. The results from these studies suggest that neurostimulation may augment improvements in both motor and cognitive deficits after brain injury. Several studies have taken this approach in animal models of TBI, showing both behavioral enhancement and biological evidence of recovery. There have been only a few studies using deep brain stimulation (DBS) in human TBI patients, and future studies are warranted to validate the feasibility of this technique in the clinical treatment of TBI. In this review, the authors summarize insights from studies employing neurostimulation techniques in the setting of brain injury. Moreover, they relate these findings to the future prospect of using DBS to ameliorate motor and cognitive deficits following TBI.

  9. Neuropsychologists diagnose traumatic brain injury.

    PubMed

    Wade, James B; DeMatteo, David; Hart, Robert P

    2004-07-01

    The case of John versus Im (2002) stands for the proposition that clinical neuropsychologists are not qualified to diagnose traumatic brain injury. This ruling by the Supreme Court of Virginia prohibits neuropsychologists from testifying about these professional conclusions in the courtroom. However, in clinical practice neuropsychologists are often asked to disentangle the relative contribution of brain dysfunction and psychological factors to presenting symptomology. In the proposed submission, the authors provide an analysis of the neuropsychological testimony at issue in John versus Im using the admissibility standards for expert testimony that were established and refined by a trilogy of cases from the Supreme Court of the United States. The paper provides support for the notion that neuropsychological method has an established scientific base of knowledge, standards for clinical competence, and evidence of peer-reviewed acceptance by medical related disciplines. No other scientific discipline has employed a more rigorous methodology for assessing cognitive function and disentangling the relative contributions of brain dysfunction and psychological factors to presenting symptomology. By limiting the testimony of neuropsychologists as to cause of an individual's cognitive impairment, courts will exclude opinions based on scientific research and specialized knowledge that would assist in the trier of fact.

  10. Endocannabinoids and traumatic brain injury

    PubMed Central

    Shohami, Esther; Cohen-Yeshurun, Ayelet; Magid, Lital; Algali, Merav; Mechoulam, Raphael

    2011-01-01

    Traumatic brain injury (TBI) represents the leading cause of death in young individuals. It triggers the accumulation of harmful mediators, leading to secondary damage, yet protective mechanisms are also set in motion. The endocannabinoid (eCB) system consists of ligands, such as anandamide and 2-arachidonoyl-glycerol (2-AG), receptors (e.g. CB1, CB2), transporters and enzymes, which are responsible for the ‘on-demand’ synthesis and degradation of these lipid mediators. There is a large body of evidence showing that eCB are markedly increased in response to pathogenic events. This fact, as well as numerous studies on experimental models of brain toxicity, neuroinflammation and trauma supports the notion that the eCB are part of the brain's compensatory or repair mechanisms. These are mediated via CB receptors signalling pathways that are linked to neuronal survival and repair. The levels of 2-AG, the most highly abundant eCB, are significantly elevated after TBI and when administered to TBI mice, 2-AG decreases brain oedema, inflammation and infarct volume and improves clinical recovery. The role of CB1 in mediating these effects was demonstrated using selective antagonists or CB1 knockout mice. CB2 were shown in other models of brain insults to reduce white blood cell rolling and adhesion, to reduce infarct size and to improve motor function. This review is focused on the role the eCB system plays as a self-neuroprotective mechanism and its potential as a basis for the development of novel therapeutic modality for the treatment of CNS pathologies with special emphasis on TBI. LINKED ARTICLES This article is part of a themed issue on Cannabinoids in Biology and Medicine. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2011.163.issue-7 PMID:21418185

  11. Seizures Following Traumatic Brain Injury in Childhood.

    ERIC Educational Resources Information Center

    Williams, Dennis

    This guide provides information on seizures in students with traumatic brain injury (TBI) and offers guidelines for classroom management. First, a classification system for seizures is presented with specific types of seizures explained. Post-traumatic seizures are specifically addressed as is the importance of seizure prevention when possible.…

  12. Traumatic brain injury among North Carolina's veterans.

    PubMed

    Hooker, James Stewart; Moore, Daniel P

    2015-04-01

    This article describes the difficulty of diagnosing traumatic brain injury (TBI), treatment protocols provided through the military, an alternative therapy with scientific evidence of its effectiveness in repairing injured brain tissue, challenges faced by brain-injured veterans seeking community reintegration, and state services that are available to help veterans.

  13. Assessment of Students with Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Chesire, David J.; Buckley, Valerie A.; Canto, Angela I.

    2011-01-01

    The incidence of brain injuries, as well as their impact on individuals who sustain them, has received growing attention from American media in recent years. This attention is likely the result of high profile individuals suffering brain injuries. Greater public awareness of traumatic brain injuries (TBIs) has also been promoted by sources such as…

  14. Aquaporin-4 and traumatic brain edema.

    PubMed

    Xu, Miao; Su, Wei; Xu, Qiu-ping

    2010-04-01

    Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: "vasogenic" and "cytotoxic/cellular". However, the cellular and molecular mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no effective drugs can be used now. Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 has been proposed as a novel drug target in brain edema. These findings suggest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.

  15. Neuroepidemiology of traumatic brain injury.

    PubMed

    Gardner, A J; Zafonte, R

    2016-01-01

    Traumatic brain injury (TBI) is a significant public-health concern. TBI is defined as an acute brain injury resulting from mechanical energy to the head from external physical forces. Some of the leading causes of TBI include falls, assaults, motor vehicle or traffic accidents, and sport-related concussion. Two of the most common identified risk factors are sex (males are nearly three times more likely to suffer a TBI than females); and a bimodal age pattern (persons 65 years and older, and children under 14 years old). It is estimated that approximately 1.5-2 million Americans suffer from TBI annually. TBIs account for around 1.4 million emergency room visits, 275 000 hospital admissions, and 52 000 deaths in the USA each year. TBI contributes to approximately 30% of all deaths in the USA annually. In Australia, it is estimated that approximately 338 700 individuals (1.9% of the population) suffer from a disability related to TBI. Of these, 160 200 were severely or profoundly affected by acquired brain injury, requiring daily support. In the UK, TBI accounted for 3.4% of all emergency department attendances annually. An overall rate of 453 per 100 000 was found for all TBI severities, of which 40 per 100 000 (10.9%) were moderate to severe. TBI often results in residual symptoms that affect an individual's cognition, movement, sensation, and/or emotional functioning. Recovery and rehabilitation from TBI may require considerable resources and may take years. Some individuals never fully recover, and some require lifetime ongoing care and support. TBI has an enormous social and financial cost, with estimates of the annual financial burden associated with TBI ranging between 9 and 10 billion US dollars. PMID:27637960

  16. Post-traumatic stress disorder vs traumatic brain injury

    PubMed Central

    Bryant, Richard

    2011-01-01

    Post-traumatic stress disorder (PTSD) and traumatic brain injury (TBI) often coexist because brain injuries are often sustained in traumatic experiences. This review outlines the significant overlap between PTSD and TBI by commencing with a critical outline of the overlapping symptoms and problems of differential diagnosis. The impact of TBI on PTSD is then described, with increasing evidence suggesting that mild TBI can increase risk for PTSD. Several explanations are offered for this enhanced risk. Recent evidence suggests that impairment secondary to mild TBI is largely attributable to stress reactions after TBI, which challenges the long-held belief that postconcussive symptoms are a function of neurological insult This recent evidence is pointing to new directions for treatment of postconcussive symptoms that acknowledge that treating stress factors following TBI may be the optimal means to manage the effects of many TBIs, PMID:22034252

  17. Brain Imaging and Behavioral Outcome in Traumatic Brain Injury.

    ERIC Educational Resources Information Center

    Bigler, Erin D.

    1996-01-01

    This review explores the cellular pathology associated with traumatic brain injury (TBI) and its relation to neurobehavioral outcomes, the relationship of brain imaging findings to underlying pathology, brain imaging techniques, various image analysis procedures and how they relate to neuropsychological testing, and the importance of brain imaging…

  18. Behavioral Considerations Associated with Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Mayfield, Joan; Homack, Susan

    2005-01-01

    Children who sustain traumatic brain injury (TBI) can experience significant cognitive deficits. These deficits may significantly impair their functioning in the classroom, resulting in the need for academic and behavioral modifications. Behavior and social problems can be the direct or indirect result of brain injury. Difficulties in paying…

  19. 45 CFR 1308.16 - Eligibility criteria: Traumatic brain injury.

    Code of Federal Regulations, 2013 CFR

    2013-10-01

    ... 45 Public Welfare 4 2013-10-01 2013-10-01 false Eligibility criteria: Traumatic brain injury. 1308... DISABILITIES Health Services Performance Standards § 1308.16 Eligibility criteria: Traumatic brain injury. A child is classified as having traumatic brain injury whose brain injuries are caused by an...

  20. 45 CFR 1308.16 - Eligibility criteria: Traumatic brain injury.

    Code of Federal Regulations, 2014 CFR

    2014-10-01

    ... 45 Public Welfare 4 2014-10-01 2014-10-01 false Eligibility criteria: Traumatic brain injury. 1308... DISABILITIES Health Services Performance Standards § 1308.16 Eligibility criteria: Traumatic brain injury. A child is classified as having traumatic brain injury whose brain injuries are caused by an...

  1. 45 CFR 1308.16 - Eligibility criteria: Traumatic brain injury.

    Code of Federal Regulations, 2011 CFR

    2011-10-01

    ... 45 Public Welfare 4 2011-10-01 2011-10-01 false Eligibility criteria: Traumatic brain injury. 1308... DISABILITIES Health Services Performance Standards § 1308.16 Eligibility criteria: Traumatic brain injury. A child is classified as having traumatic brain injury whose brain injuries are caused by an...

  2. 45 CFR 1308.16 - Eligibility criteria: Traumatic brain injury.

    Code of Federal Regulations, 2012 CFR

    2012-10-01

    ... 45 Public Welfare 4 2012-10-01 2012-10-01 false Eligibility criteria: Traumatic brain injury. 1308... DISABILITIES Health Services Performance Standards § 1308.16 Eligibility criteria: Traumatic brain injury. A child is classified as having traumatic brain injury whose brain injuries are caused by an...

  3. 45 CFR 1308.16 - Eligibility criteria: Traumatic brain injury.

    Code of Federal Regulations, 2010 CFR

    2010-10-01

    ... 45 Public Welfare 4 2010-10-01 2010-10-01 false Eligibility criteria: Traumatic brain injury. 1308... DISABILITIES Health Services Performance Standards § 1308.16 Eligibility criteria: Traumatic brain injury. A child is classified as having traumatic brain injury whose brain injuries are caused by an...

  4. Hypothermia following Pediatric Traumatic Brain Injury

    PubMed Central

    2009-01-01

    Abstract Preclinical as well as clinical studies in traumatic brain injury (TBI) have established the likely association of secondary injury and outcome in adults in children following severe injury. Similarly, there is growing evidence in experimental laboratory studies that moderate hypothermia has a beneficial effect on outcome, though the exact mechanisms remain to be absolutely defined. The Pediatric TBI Guidelines provided the knowledge and background for standard management of children following severe TBI and highlighted that there are very few clinical studies to date. In particular with respect to temperature regulation and the use of hypothermia, initial findings of case series of small numbers were promising. Further preliminary randomized clinical trials, both single institution and multicenter, have provided the initial data on safety and efficacy, though larger, Phase III studies are necessary to ensure both the safety and efficacy of hypothermia in pediatric TBI prior to implementation as part of the standard of care. It is expected that hypothermia initiated early after severe TBI will have a protective effect on the pediatric brain and can be done safely, but this still remains to be definitively tested. PMID:19271965

  5. Surveillance of traumatic brain injuries in Utah.

    PubMed Central

    Thurman, D J; Jeppson, L; Burnett, C L; Beaudoin, D E; Rheinberger, M M; Sniezek, J E

    1996-01-01

    From 1990 through 1992 we conducted surveillance of cases requiring hospital admission and of fatal cases of traumatic brain injury among residents of Utah and found an annual incidence rate of 108.8 per 100,000 population. The greatest number of injuries occurred among men and persons aged 15 to 24 years. Motor vehicles were the leading cause of injury, followed by falls and assaults. The incidence rate we found is substantially lower than previously published rates of traumatic brain injury. This may be the result of a decrease in the incidence of these injuries in the decade since earlier studies were done, as well as changing hospital admission criteria that serve to exclude less severe cases of injury. Despite the apparent decline in rates, our findings indicate the continued importance of traumatic brain injury as a public health problem and the need to develop more effective prevention strategies that will address the major causes of these injuries. PMID:8987423

  6. Defense Centers of Excellence for Psychological Health & Traumatic Brain Injury

    MedlinePlus

    Skip Navigation Sign up Search: Defense Centers of Excellence For Psychological Health & Traumatic Brain Injury U.S. Department ... Section 508 External Link Disclaimer Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury | 800- ...

  7. Post-traumatic stress disorder and traumatic brain injury.

    PubMed

    Motzkin, Julian C; Koenigs, Michael R

    2015-01-01

    Disentangling the effects of "organic" neurologic damage and psychological distress after a traumatic brain injury poses a significant challenge to researchers and clinicians. Establishing a link between traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) has been particularly contentious, reflecting difficulties in establishing a unique diagnosis for conditions with overlapping and sometimes contradictory symptom profiles. However, each disorder is linked to a variety of adverse health outcomes, underscoring the need to better understand how neurologic and psychiatric risk factors interact following trauma. Here, we present data showing that individuals with a TBI are more likely to develop PTSD, and that individuals with PTSD are more likely to develop persistent cognitive sequelae related to TBI. Further, we describe neurobiological models of PTSD, highlighting how patterns of neurologic damage typical in TBI may promote or protect against the development of PTSD in brain-injured populations. These data highlight the unique course of PTSD following a TBI and have important diagnostic, prognostic, and treatment implications for individuals with a dual diagnosis.

  8. Clinimetric measurement in traumatic brain injuries.

    PubMed

    Opara, J A; Małecka, E; Szczygiel, J

    2014-06-15

    Traumatic brain injury is a leading cause of death and disability worldwide. Every year, about 1.5 million affected people die and several millions receive emergency treatment. Most of the burden (90%) is in low and middle-income countries. The costs of care depend on the level of disability. The burden of care after traumatic brain injury is caused by disability as well as by psychosocial and emotional sequelae of injury. The final consequence of brain injury is the reduction of quality of life. It is very difficult to predict the outcome after traumatic brain injury. The basic clinical model included four predictors: age, score in Glasgow coma scale, pupil reactivity, and the presence of major extracranial injury. These are the neuroradiological markers of recovery after TBI (CT, MRI and PET) and biomarkers: genetic markers of ApoE Gene, ectoenzyme CD 38 (cluster of differentiation 38), serum S100B, myelin basic protein (MBP), neuron specific endolase (NSE), and glial fibrillary acidic protein (GPAP). These are many clinimetric scales which are helpful in prognosing after head injury. In this review paper, the most commonly used scales evaluating the level of consciousness after traumatic brain injury have been presented.

  9. Mild Traumatic Brain Injury in Translation

    PubMed Central

    Robertson, Claudia S.

    2013-01-01

    Abstract This Introduction to a Special Issue on Mild Traumatic Brain Injury (mTBI) highlights the methodological challenges in outcome studies and clinical trials involving patients who sustain mTBI. Recent advances in brain imaging and portable, computerized cognitive tasks have contributed to protocols that are sensitive to the effects of mTBI and efficient in time for completion. Investigation of civilian mTBI has been extended to single and repeated injuries in athletes and blast-related mTBI in service members and veterans. Despite differences in mechanism of injury, there is evidence for similar effects of acceleration-deceleration and blast mechanisms of mTBI on cognition. Investigation of repetitive mTBI suggests that the effects may be cumulative and that repeated mTBI and repeated subconcussive head trauma may lead to neurodegenerative conditions. Although animal models of mTBI using cortical impact and fluid percussion injury in rodents have been able to reproduce some of the cognitive deficits frequently exhibited by patients after mTBI, modeling post-concussion symptoms is difficult. Recent use of closed head and blast injury animal models may more closely approximate clinical mTBI. Translation of interventions that are developed in animal models to patients with mTBI is a priority for the research agenda. This Special Issue on mTBI integrates basic neuroscience studies using animal models with studies of human mTBI, including the cognitive sequelae, persisting symptoms, brain imaging, and host factors that facilitate recovery. PMID:23046349

  10. Discriminating military and civilian traumatic brain injuries.

    PubMed

    Reid, Matthew W; Velez, Carmen S

    2015-05-01

    Traumatic brain injury (TBI) occurs at higher rates among service members than civilians. Explosions from improvised explosive devices and mines are the leading cause of TBI in the military. As such, TBI is frequently accompanied by other injuries, which makes its diagnosis and treatment difficult. In addition to postconcussion symptoms, those who sustain a TBI commonly report chronic pain and posttraumatic stress symptoms. This combination of symptoms is so typical they have been referred to as the "polytrauma clinical triad" among injured service members. We explore whether these symptoms discriminate civilian occurrences of TBI from those of service members, as well as the possibility that repeated blast exposure contributes to the development of chronic traumatic encephalopathy (CTE). This article is part of a Special Issue entitled 'Traumatic Brain Injury'.

  11. Subacute to chronic mild traumatic brain injury.

    PubMed

    Mott, Timothy F; McConnon, Michael L; Rieger, Brian P

    2012-12-01

    Although a universally accepted definition is lacking, mild traumatic brain injury and concussion are classified by transient loss of consciousness, amnesia, altered mental status, a Glasgow Coma Score of 13 to 15, and focal neurologic deficits following an acute closed head injury. Most patients recover quickly, with a predictable clinical course of recovery within the first one to two weeks following traumatic brain injury. Persistent physical, cognitive, or behavioral postconcussive symptoms may be noted in 5 to 20 percent of persons who have mild traumatic brain injury. Physical symptoms include headaches, dizziness, and nausea, and changes in coordination, balance, appetite, sleep, vision, and hearing. Cognitive and behavioral symptoms include fatigue, anxiety, depression, and irritability, and problems with memory, concentration and decision making. Women, older adults, less educated persons, and those with a previous mental health diagnosis are more likely to have persistent symptoms. The diagnostic workup for subacute to chronic mild traumatic brain injury focuses on the history and physical examination, with continuing observation for the development of red flags such as the progression of physical, cognitive, and behavioral symptoms, seizure, progressive vomiting, and altered mental status. Early patient and family education should include information on diagnosis and prognosis, symptoms, and further injury prevention. Symptom-specific treatment, gradual return to activity, and multidisciplinary coordination of care lead to the best outcomes. Psychiatric and medical comorbidities, psychosocial issues, and legal or compensatory incentives should be explored in patients resistant to treatment.

  12. Traumatic Brain Injury and Personality Change

    ERIC Educational Resources Information Center

    Fowler, Marc; McCabe, Paul C.

    2011-01-01

    Traumatic brain injury (TBI) is the leading cause of death and lifelong disability in the United States for individuals below the age of 45. Current estimates from the Center for Disease Control (CDC) indicate that at least 1.4 million Americans sustain a TBI annually. TBI affects 475,000 children under age 14 each year in the United States alone.…

  13. Traumatic Brain Injury: Perspectives from Educational Professionals

    ERIC Educational Resources Information Center

    Mohr, J. Darrell; Bullock, Lyndal M.

    2005-01-01

    This article reports the outcomes from 2 focus groups conducted to ascertain professional educators' perceptions regarding their (a) level of preparedness for working with students with traumatic brain injury (TBI), (b) ideas regarding ways to improve support to students and families, and (c) concerns about meeting the diverse needs of children…

  14. Reality Lessons in Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Adams, Elaine Parker; Adams, Albert A., Jr.

    2008-01-01

    This article goes beyond the typical guidance on how to address the educational needs of students with traumatic brain injury (TBI). A survivor of TBI and his parent advocate describe real-life encounters in the education arena and offer ways to respond to the problems depicted in the situations. Their candor enhances educator awareness of the…

  15. School Reentry Following Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Deidrick, Kathleen K. M.; Farmer, Janet E.

    2005-01-01

    Successful school reentry following traumatic brain injury (TBI) is critical to recovery. Physical, cognitive, behavioral, academic, and social problems can affect a child's school performance after a TBI. However, early intervention has the potential to improve child academic outcomes and promote effective coping with any persistent changes in…

  16. Traumatic Brain Injury and Vocational Rehabilitation.

    ERIC Educational Resources Information Center

    Corthell, David W., Ed.

    Intended to serve as a resource guide on traumatic brain injury for rehabilitation practitioners, the book's 10 chapters are grouped into sections which provide an introduction and examine aspects of evaluation, treatment and placement planning, and unresolved issues. Chapters have the following titles and authors: "Scope of the Problem" (Marilyn…

  17. Subacute to chronic mild traumatic brain injury.

    PubMed

    Mott, Timothy F; McConnon, Michael L; Rieger, Brian P

    2012-12-01

    Although a universally accepted definition is lacking, mild traumatic brain injury and concussion are classified by transient loss of consciousness, amnesia, altered mental status, a Glasgow Coma Score of 13 to 15, and focal neurologic deficits following an acute closed head injury. Most patients recover quickly, with a predictable clinical course of recovery within the first one to two weeks following traumatic brain injury. Persistent physical, cognitive, or behavioral postconcussive symptoms may be noted in 5 to 20 percent of persons who have mild traumatic brain injury. Physical symptoms include headaches, dizziness, and nausea, and changes in coordination, balance, appetite, sleep, vision, and hearing. Cognitive and behavioral symptoms include fatigue, anxiety, depression, and irritability, and problems with memory, concentration and decision making. Women, older adults, less educated persons, and those with a previous mental health diagnosis are more likely to have persistent symptoms. The diagnostic workup for subacute to chronic mild traumatic brain injury focuses on the history and physical examination, with continuing observation for the development of red flags such as the progression of physical, cognitive, and behavioral symptoms, seizure, progressive vomiting, and altered mental status. Early patient and family education should include information on diagnosis and prognosis, symptoms, and further injury prevention. Symptom-specific treatment, gradual return to activity, and multidisciplinary coordination of care lead to the best outcomes. Psychiatric and medical comorbidities, psychosocial issues, and legal or compensatory incentives should be explored in patients resistant to treatment. PMID:23198672

  18. Understanding Traumatic Brain Injury: An Introduction

    ERIC Educational Resources Information Center

    Trudel, Tina M.; Scherer, Marcia J.; Elias, Eileen

    2009-01-01

    This article is the first of a multi-part series on traumatic brain injury (TBI). Historically, TBI has received very limited national public policy attention and support. However since it has become the signature injury of the military conflicts in Iraq and Afghanistan, TBI has gained the attention of elected officials, military leaders,…

  19. Working with Students with Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Lucas, Matthew D.

    2010-01-01

    The participation of a student with Traumatic Brain Injury (TBI) in general physical education can often be challenging and rewarding for the student and physical education teacher. This article addresses common characteristics of students with TBI and presents basic solutions to improve the education of students with TBI in the general physical…

  20. Traumatic Brain Injury: Looking Back, Looking Forward

    ERIC Educational Resources Information Center

    Bartlett, Sue; Lorenz, Laura; Rankin, Theresa; Elias, Eileen; Weider, Katie

    2011-01-01

    This article is the eighth of a multi-part series on traumatic brain injury (TBI). Historically, TBI has received limited national attention and support. However, since it is the signature injury of the military conflicts in Iraq and Afghanistan, TBI has gained attention of elected officials, military leaders, policymakers, and the public. The…

  1. Narrative Language in Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Marini, Andrea; Galetto, Valentina; Zampieri, Elisa; Vorano, Lorenza; Zettin, Marina; Carlomagno, Sergio

    2011-01-01

    Persons with traumatic brain injury (TBI) often show impaired linguistic and/or narrative abilities. The present study aimed to document the features of narrative discourse impairment in a group of adults with TBI. 14 severe TBI non-aphasic speakers (GCS less than 8) in the phase of neurological stability and 14 neurologically intact participants…

  2. Use of magnesium in traumatic brain injury.

    PubMed

    Sen, Ananda P; Gulati, Anil

    2010-01-01

    Depletion of magnesium is observed in animal brain and in human blood after brain injury. Treatment with magnesium attenuates the pathological and behavioral changes in rats with brain injury; however, the therapeutic effect of magnesium has not been consistently observed in humans with traumatic brain injury (TBI). Secondary brain insults are observed in patients with brain injury, which adversely affect clinical outcome. Systemic administration studies in rats have shown that magnesium enters the brain; however, inducing hypermagnesemia in humans did not concomitantly increase magnesium levels in the CSF. We hypothesize that the neuroprotective effects of magnesium in TBI patients could be observed by increasing its brain bioavailability with mannitol. Here, we review the role of magnesium in brain injury, preclinical studies in brain injury, clinical safety and efficacy studies in TBI patients, brain bioavailability studies in rat, and pharmacokinetic studies in humans with brain injury. Neurodegeneration after brain injury involves multiple biochemical pathways. Treatment with a single agent has often resulted in poor efficacy at a safe dose or toxicity at a therapeutic dose. A successful neuroprotective therapy needs to be aimed at homeostatic control of these pathways with multiple agents. Other pharmacological agents, such as dexanabinol and progesterone, and physiological interventions, with hypothermia and hyperoxia, have been studied for the treatment of brain injury. Treatment with magnesium and hypothermia has shown favorable outcome in rats with cerebral ischemia. We conclude that coadministration of magnesium and mannitol with pharmacological and physiological agents could be an effective neuroprotective regimen for the treatment of TBI. PMID:20129501

  3. The costs of traumatic brain injury: a literature review

    PubMed Central

    Humphreys, Ioan; Wood, Rodger L; Phillips, Ceri J; Macey, Steven

    2013-01-01

    Objective The purpose of this study was to review the literature relating to the psychosocial costs associated with traumatic brain injury (TBI). Methods Nine online journal databases, including MEDLINE, CINAHL, PsychINFO, and PUBMED, were queried for studies between July 2010 and May 2012 pertaining to the economic burden of head injuries. Additional studies were identified through searching bibliographies of related publications and using Google internet search engine. Results One hundred and eight potentially relevant abstracts were identified from the journal databases. Ten papers were chosen for discussion in this review. All but two of the chosen papers were US studies. The studies included a cost-benefit analysis of the implementation of treatment guidelines from the US brain trauma foundation and a cost-effectiveness analysis of post-acute traumatic brain injury rehabilitation. Conclusion Very little research has been published on the economic burden that mild and moderate traumatic brain injury patients pose to their families, careers, and society as a whole. Further research is needed to estimate the economic burden of these patients on healthcare providers and social services and how this can impact current health policies and practices. PMID:23836998

  4. Catecholamines and cognition after traumatic brain injury.

    PubMed

    Jenkins, Peter O; Mehta, Mitul A; Sharp, David J

    2016-09-01

    Cognitive problems are one of the main causes of ongoing disability after traumatic brain injury. The heterogeneity of the injuries sustained and the variability of the resulting cognitive deficits makes treating these problems difficult. Identifying the underlying pathology allows a targeted treatment approach aimed at cognitive enhancement. For example, damage to neuromodulatory neurotransmitter systems is common after traumatic brain injury and is an important cause of cognitive impairment. Here, we discuss the evidence implicating disruption of the catecholamines (dopamine and noradrenaline) and review the efficacy of catecholaminergic drugs in treating post-traumatic brain injury cognitive impairments. The response to these therapies is often variable, a likely consequence of the heterogeneous patterns of injury as well as a non-linear relationship between catecholamine levels and cognitive functions. This individual variability means that measuring the structure and function of a person's catecholaminergic systems is likely to allow more refined therapy. Advanced structural and molecular imaging techniques offer the potential to identify disruption to the catecholaminergic systems and to provide a direct measure of catecholamine levels. In addition, measures of structural and functional connectivity can be used to identify common patterns of injury and to measure the functioning of brain 'networks' that are important for normal cognitive functioning. As the catecholamine systems modulate these cognitive networks, these measures could potentially be used to stratify treatment selection and monitor response to treatment in a more sophisticated manner.

  5. Catecholamines and cognition after traumatic brain injury

    PubMed Central

    Jenkins, Peter O.; Mehta, Mitul A.

    2016-01-01

    Cognitive problems are one of the main causes of ongoing disability after traumatic brain injury. The heterogeneity of the injuries sustained and the variability of the resulting cognitive deficits makes treating these problems difficult. Identifying the underlying pathology allows a targeted treatment approach aimed at cognitive enhancement. For example, damage to neuromodulatory neurotransmitter systems is common after traumatic brain injury and is an important cause of cognitive impairment. Here, we discuss the evidence implicating disruption of the catecholamines (dopamine and noradrenaline) and review the efficacy of catecholaminergic drugs in treating post-traumatic brain injury cognitive impairments. The response to these therapies is often variable, a likely consequence of the heterogeneous patterns of injury as well as a non-linear relationship between catecholamine levels and cognitive functions. This individual variability means that measuring the structure and function of a person’s catecholaminergic systems is likely to allow more refined therapy. Advanced structural and molecular imaging techniques offer the potential to identify disruption to the catecholaminergic systems and to provide a direct measure of catecholamine levels. In addition, measures of structural and functional connectivity can be used to identify common patterns of injury and to measure the functioning of brain ‘networks’ that are important for normal cognitive functioning. As the catecholamine systems modulate these cognitive networks, these measures could potentially be used to stratify treatment selection and monitor response to treatment in a more sophisticated manner. PMID:27256296

  6. Catecholamines and cognition after traumatic brain injury.

    PubMed

    Jenkins, Peter O; Mehta, Mitul A; Sharp, David J

    2016-09-01

    Cognitive problems are one of the main causes of ongoing disability after traumatic brain injury. The heterogeneity of the injuries sustained and the variability of the resulting cognitive deficits makes treating these problems difficult. Identifying the underlying pathology allows a targeted treatment approach aimed at cognitive enhancement. For example, damage to neuromodulatory neurotransmitter systems is common after traumatic brain injury and is an important cause of cognitive impairment. Here, we discuss the evidence implicating disruption of the catecholamines (dopamine and noradrenaline) and review the efficacy of catecholaminergic drugs in treating post-traumatic brain injury cognitive impairments. The response to these therapies is often variable, a likely consequence of the heterogeneous patterns of injury as well as a non-linear relationship between catecholamine levels and cognitive functions. This individual variability means that measuring the structure and function of a person's catecholaminergic systems is likely to allow more refined therapy. Advanced structural and molecular imaging techniques offer the potential to identify disruption to the catecholaminergic systems and to provide a direct measure of catecholamine levels. In addition, measures of structural and functional connectivity can be used to identify common patterns of injury and to measure the functioning of brain 'networks' that are important for normal cognitive functioning. As the catecholamine systems modulate these cognitive networks, these measures could potentially be used to stratify treatment selection and monitor response to treatment in a more sophisticated manner. PMID:27256296

  7. Traumatic Brain Injury Due to Bull Assault in a Girl: a Case Report

    PubMed Central

    ALVIS-MIRANDA, Hernando Raphael; CASTELLAR-LEONES, Sandra Milena; VELÁSQUEZ-LOPERENA, Dufays Danith; VILLA-DELGADO, Rosmery; ALCALA-CERRA, Gabriel; MOSCOTE-SALAZAR, Luis Rafael

    2013-01-01

    ABSTRACT Traumatic brain injury is a common condition in the emergency services, affecting the pediatric and adult population significantly. Patterns of head injury as well as management principles in children are important differences compared to adults. Traumatic brain injury by bull rush is usually seen in adults but has not been described in children-report a pediatric cranial trauma present bull rush, which to our knowledge is the first report in the literature of this nature. PMID:24790672

  8. Traumatic brain injury and criminal behaviour.

    PubMed

    Diaz, F G

    1995-01-01

    The clinical characteristics of traumatic brain injury (TBI), the association of TBI with lasting behavioural problems and neuropsychological deficits, and the use of the insanity defense in criminal proceedings in relation to TBI are discussed. Furthermore, the possible abuse of the incidental association of a TBI to the commission of a crime is explored. A framework of evaluation is described to determine the relevance of the association of TBI and the ultimate commission of a crime.

  9. Managing traumatic brain injury secondary to explosions

    PubMed Central

    Burgess, Paula; E Sullivent, Ernest; M Sasser, Scott; M Wald, Marlena; Ossmann, Eric; Kapil, Vikas

    2010-01-01

    Explosions and bombings are the most common deliberate cause of disasters with large numbers of casualties. Despite this fact, disaster medical response training has traditionally focused on the management of injuries following natural disasters and terrorist attacks with biological, chemical, and nuclear agents. The following article is a clinical primer for physicians regarding traumatic brain injury (TBI) caused by explosions and bombings. The history, physics, and treatment of TBI are outlined. PMID:20606794

  10. The prehospital management of traumatic brain injury.

    PubMed

    Goldberg, Scott A; Rojanasarntikul, Dhanadol; Jagoda, Andrew

    2015-01-01

    Traumatic brain injury (TBI) is an important cause of death and disability, particularly in younger populations. The prehospital evaluation and management of TBI is a vital link between insult and definitive care and can have dramatic implications for subsequent morbidity. Following a TBI the brain is at high risk for further ischemic injury, with prehospital interventions targeted at reducing this secondary injury while optimizing cerebral physiology. In the following chapter we discuss the prehospital assessment and management of the brain-injured patient. The initial evaluation and physical examination are discussed with a focus on interpretation of specific physical examination findings and interpretation of vital signs. We evaluate patient management strategies including indications for advanced airway management, oxygenation, ventilation, and fluid resuscitation, as well as prehospital strategies for the management of suspected or impending cerebral herniation including hyperventilation and brain-directed hyperosmolar therapy. Transport decisions including the role of triage models and trauma centers are discussed. Finally, future directions in the prehospital management of traumatic brain injury are explored.

  11. Neurobiological consequences of traumatic brain injury

    PubMed Central

    McAllister, Thomas W.

    2011-01-01

    Traumatic brain injury (TBI) is a worldwide public health problem typically caused by contact and inertial forces acting on the brain. Recent attention has also focused on the mechanisms of injury associated with exposure to blast events or explosions. Advances in the understanding of the neuropathophysiology of TBI suggest that these forces initiate an elaborate and complex array of cellular and subcellular events related to alterations in Ca++ homeostasis and signaling. Furthermore, there is a fairly predictable profile of brain regions that are impacted by neurotrauma and the related events. This profile of brain damage accurately predicts the acute and chronic sequelae that TBI survivors suffer from, although there is enough variation to suggest that individual differences such as genetic polymorphisms and factors governing resiliency play a role in modulating outcome. This paper reviews our current understanding of the neuropathophysiology of TBI and how this relates to the common clinical presentation of neurobehavioral difficulties seen after an injury. PMID:22033563

  12. Traumatic brain injury and forensic neuropsychology.

    PubMed

    Bigler, Erin D; Brooks, Michael

    2009-01-01

    As part of a special issue of The Journal of Head Trauma Rehabilitation, forensic neuropsychology is reviewed as it applies to traumatic brain injury (TBI) and other types of acquired brain injury in which clinical neuropsychologists and rehabilitation psychologists may be asked to render professional opinions about the neurobehavioral effects and outcome of a brain injury. The article introduces and overviews the topic focusing on the process of forensic neuropsychological consultation and practice as it applies to patients with TBI or other types of acquired brain injury. The emphasis is on the application of scientist-practitioner standards as they apply to legal questions about the status of a TBI patient and how best that may be achieved. This article introduces each topic area covered in this special edition.

  13. Traumatic Brain Injury: An Educator's Manual. [Revised Edition.

    ERIC Educational Resources Information Center

    Fiegenbaum, Ed, Ed.; And Others

    This manual for the Portland (Oregon) Public Schools presents basic information on providing educational services to children with traumatic brain injury (TBI). Individual sections cover the following topics: the brain, central nervous system and behavior; physical, psychological and emotional implication; traumatic brain injury in children versus…

  14. Traumatic Brain Injury as a Cause of Behavior Disorders.

    ERIC Educational Resources Information Center

    Nordlund, Marcia R.

    There is increasing evidence that many children and adolescents who display behavior disorders have sustained a traumatic brain injury. Traumatic brain injury can take the following forms: closed head trauma in which the brain usually suffers diffuse damage; open head injury which usually results in specific focal damage; or internal trauma (e.g.,…

  15. Traumatic Brain Injury and Sleep Disorders

    PubMed Central

    Viola-Saltzman, Mari; Watson, Nathaniel F.

    2012-01-01

    SYNOPSIS Sleep disturbance is common following traumatic brain injury (TBI), affecting 30–70% of individuals, many occurring after mild injuries. Insomnia, fatigue and sleepiness are the most frequent post-TBI sleep complaints with narcolepsy (with or without cataplexy), sleep apnea (obstructive and/or central), periodic limb movement disorder, and parasomnias occurring less commonly. In addition, depression, anxiety and pain are common TBI co-morbidities with substantial influence on sleep quality. Two types of TBI negatively impact sleep: contact injuries causing focal brain damage and acceleration/deceleration injuries causing more generalized brain damage. Diagnosis of sleep disorders after TBI may involve polysomnography, multiple sleep latency testing and/or actigraphy. Treatment is disorder specific and may include the use of medications, continuous positive airway pressure (or similar device) and/or behavioral modifications. Unfortunately, treatment of sleep disorders associated with TBI often does not improve sleepiness or neuropsychological function. PMID:23099139

  16. Chronic cerebrovascular dysfunction after traumatic brain injury.

    PubMed

    Jullienne, Amandine; Obenaus, Andre; Ichkova, Aleksandra; Savona-Baron, Catherine; Pearce, William J; Badaut, Jerome

    2016-07-01

    Traumatic brain injuries (TBI) often involve vascular dysfunction that leads to long-term alterations in physiological and cognitive functions of the brain. Indeed, all the cells that form blood vessels and that are involved in maintaining their proper function can be altered by TBI. This Review focuses on the different types of cerebrovascular dysfunction that occur after TBI, including cerebral blood flow alterations, autoregulation impairments, subarachnoid hemorrhage, vasospasms, blood-brain barrier disruption, and edema formation. We also discuss the mechanisms that mediate these dysfunctions, focusing on the cellular components of cerebral blood vessels (endothelial cells, smooth muscle cells, astrocytes, pericytes, perivascular nerves) and their known and potential roles in the secondary injury cascade. © 2016 Wiley Periodicals, Inc. PMID:27117494

  17. Traumatic brain injury, neuroimaging, and neurodegeneration

    PubMed Central

    Bigler, Erin D.

    2012-01-01

    Depending on severity, traumatic brain injury (TBI) induces immediate neuropathological effects that in the mildest form may be transient but as severity increases results in neural damage and degeneration. The first phase of neural degeneration is explainable by the primary acute and secondary neuropathological effects initiated by the injury; however, neuroimaging studies demonstrate a prolonged period of pathological changes that progressively occur even during the chronic phase. This review examines how neuroimaging may be used in TBI to understand (1) the dynamic changes that occur in brain development relevant to understanding the effects of TBI and how these relate to developmental stage when the brain is injured, (2) how TBI interferes with age-typical brain development and the effects of aging thereafter, and (3) how TBI results in greater frontotemporolimbic damage, results in cerebral atrophy, and is more disruptive to white matter neural connectivity. Neuroimaging quantification in TBI demonstrates degenerative effects from brain injury over time. An adverse synergistic influence of TBI with aging may predispose the brain injured individual for the development of neuropsychiatric and neurodegenerative disorders long after surviving the brain injury. PMID:23964217

  18. Traumatic brain injury, neuroimaging, and neurodegeneration.

    PubMed

    Bigler, Erin D

    2013-01-01

    Depending on severity, traumatic brain injury (TBI) induces immediate neuropathological effects that in the mildest form may be transient but as severity increases results in neural damage and degeneration. The first phase of neural degeneration is explainable by the primary acute and secondary neuropathological effects initiated by the injury; however, neuroimaging studies demonstrate a prolonged period of pathological changes that progressively occur even during the chronic phase. This review examines how neuroimaging may be used in TBI to understand (1) the dynamic changes that occur in brain development relevant to understanding the effects of TBI and how these relate to developmental stage when the brain is injured, (2) how TBI interferes with age-typical brain development and the effects of aging thereafter, and (3) how TBI results in greater frontotemporolimbic damage, results in cerebral atrophy, and is more disruptive to white matter neural connectivity. Neuroimaging quantification in TBI demonstrates degenerative effects from brain injury over time. An adverse synergistic influence of TBI with aging may predispose the brain injured individual for the development of neuropsychiatric and neurodegenerative disorders long after surviving the brain injury.

  19. Pediatric Rodent Models of Traumatic Brain Injury.

    PubMed

    Semple, Bridgette D; Carlson, Jaclyn; Noble-Haeusslein, Linda J

    2016-01-01

    Due to a high incidence of traumatic brain injury (TBI) in children and adolescents, age-specific studies are necessary to fully understand the long-term consequences of injuries to the immature brain. Preclinical and translational research can help elucidate the vulnerabilities of the developing brain to insult, and provide model systems to formulate and evaluate potential treatments aimed at minimizing the adverse effects of TBI. Several experimental TBI models have therefore been scaled down from adult rodents for use in juvenile animals. The following chapter discusses these adapted models for pediatric TBI, and the importance of age equivalence across species during model development and interpretation. Many neurodevelopmental processes are ongoing throughout childhood and adolescence, such that neuropathological mechanisms secondary to a brain insult, including oxidative stress, metabolic dysfunction and inflammation, may be influenced by the age at the time of insult. The long-term evaluation of clinically relevant functional outcomes is imperative to better understand the persistence and evolution of behavioral deficits over time after injury to the developing brain. Strategies to modify or protect against the chronic consequences of pediatric TBI, by supporting the trajectory of normal brain development, have the potential to improve quality of life for brain-injured children. PMID:27604726

  20. Paclitaxel improves outcome from traumatic brain injury

    PubMed Central

    Cross, Donna J.; Garwin, Gregory G.; Cline, Marcella M.; Richards, Todd L.; Yarnykh, Vasily; Mourad, Pierre D.; Ho, Rodney J.Y.; Minoshima, Satoshi

    2016-01-01

    Pharmacologic interventions for traumatic brain injury (TBI) hold promise to improve outcome. The purpose of this study was to determine if the microtubule stabilizing therapeutic paclitaxel used for more than 20 years in chemotherapy would improve outcome after TBI. We assessed neurological outcome in mice that received direct application of paclitaxel to brain injury from controlled cortical impact (CCI). Magnetic resonance imaging was used to assess injury-related morphological changes. Catwalk Gait analysis showed significant improvement in the paclitaxel group on a variety of parameters compared to the saline group. MRI analysis revealed that paclitaxel treatment resulted in significantly reduced edema volume at site-of-injury (11.92 ± 3.0 and 8.86 ± 2.2 mm3 for saline vs. paclitaxel respectively, as determined by T2-weighted analysis; p ≤ 0.05), and significantly increased myelin tissue preservation (9.45 ± 0.4 vs. 8.95 ± 0.3, p ≤ 0.05). Our findings indicate that paclitaxel treatment resulted in improvement of neurological outcome and MR imaging biomarkers of injury. These results could have a significant impact on therapeutic developments to treat traumatic brain injury. PMID:26086366

  1. Prehospital management of traumatic brain injury.

    PubMed

    Stiver, Shirley I; Manley, Geoffrey T

    2008-10-01

    The aim of this study was to review the current protocols of prehospital practice and their impact on outcome in the management of traumatic brain injury. A literature review of the National Library of Medicine encompassing the years 1980 to May 2008 was performed. The primary impact of a head injury sets in motion a cascade of secondary events that can worsen neurological injury and outcome. The goals of care during prehospital triage, stabilization, and transport are to recognize life-threatening raised intracranial pressure and to circumvent cerebral herniation. In that process, prevention of secondary injury and secondary insults is a major determinant of both short- and longterm outcome. Management of brain oxygenation, blood pressure, cerebral perfusion pressure, and raised intracranial pressure in the prehospital setting are discussed. Patient outcomes are dependent upon an organized trauma response system. Dispatch and transport timing, field stabilization, modes of transport, and destination levels of care are addressed. In addition, special considerations for mass casualty and disaster planning are outlined and recommendations are made regarding early response efforts and the ethical impact of aggressive prehospital resuscitation. The most sophisticated of emergency, operative, or intensive care units cannot reverse damage that has been set in motion by suboptimal protocols of triage and resuscitation, either at the injury scene or en route to the hospital. The quality of prehospital care is a major determinant of long-term outcome for patients with traumatic brain injury.

  2. Traumatic brain injury in modern war

    NASA Astrophysics Data System (ADS)

    Ling, Geoffrey S. F.; Hawley, Jason; Grimes, Jamie; Macedonia, Christian; Hancock, James; Jaffee, Michael; Dombroski, Todd; Ecklund, James M.

    2013-05-01

    Traumatic brain injury (TBI) is common and especially with military service. In Iraq and Afghanistan, explosive blast related TBI has become prominent and is mainly from improvised explosive devices (IED). Civilian standard of care clinical practice guidelines (CPG) were appropriate has been applied to the combat setting. When such CPGs do not exist or are not applicable, new practice standards for the military are created, as for TBI. Thus, CPGs for prehospital care of combat TBI CPG [1] and mild TBI/concussion [2] were introduced as was a DoD system-wide clinical care program, the first large scale system wide effort to address all severities of TBI in a comprehensive organized way. As TBI remains incompletely understood, substantial research is underway. For the DoD, leading this effort are The Defense and Veterans Brain Injury Center, National Intrepid Center of Excellence and the Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury. This program is a beginning, a work in progress ready to leverage advances made scientifically and always with the intent of providing the best care to its military beneficiaries.

  3. Sports-related traumatic brain injury.

    PubMed

    Phillips, Shawn; Woessner, Derek

    2015-06-01

    Concussions have garnered more attention in the medical literature, media, and social media. As such, in the nomenclature according to the Centers for Disease Control and Prevention, the term concussion has been supplanted by the term mild traumatic brain injury. Current numbers indicate that 1.7 million TBIs are documented annually, with estimates around 3 million annually (173,285 sports- and recreation-related TBIs among children and adolescents). The Sideline Concussion Assessment Tool 3 and the NFL Sideline Concussion Assessment Tool are commonly used sideline tools.

  4. Imaging Evaluation of Acute Traumatic Brain Injury.

    PubMed

    Mutch, Christopher A; Talbott, Jason F; Gean, Alisa

    2016-10-01

    Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Imaging plays an important role in the evaluation, diagnosis, and triage of patients with TBI. Recent studies suggest that it also helps predict patient outcomes. TBI consists of multiple pathoanatomic entities. This article reviews the current state of TBI imaging including its indications, benefits and limitations of the modalities, imaging protocols, and imaging findings for each of these pathoanatomic entities. Also briefly surveyed are advanced imaging techniques, which include several promising areas of TBI research. PMID:27637393

  5. Diabetes Insipidus after Traumatic Brain Injury

    PubMed Central

    Capatina, Cristina; Paluzzi, Alessandro; Mitchell, Rosalid; Karavitaki, Niki

    2015-01-01

    Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in many age groups. Neuroendocrine dysfunction has been recognized as a consequence of TBI and consists of both anterior and posterior pituitary insufficiency; water and electrolyte abnormalities (diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH)) are amongst the most challenging sequelae. The acute head trauma can lead (directly or indirectly) to dysfunction of the hypothalamic neurons secreting antidiuretic hormone (ADH) or of the posterior pituitary gland causing post-traumatic DI (PTDI). PTDI is usually diagnosed in the first days after the trauma presenting with hypotonic polyuria. Frequently, the poor general status of most patients prevents adequate fluid intake to compensate the losses and severe dehydration and hypernatremia occur. Management consists of careful monitoring of fluid balance and hormonal replacement. PTDI is associated with high mortality, particularly when presenting very early following the injury. In many surviving patients, the PTDI is transient, lasting a few days to a few weeks and in a minority of cases, it is permanent requiring management similar to that offered to patients with non-traumatic central DI. PMID:26239685

  6. Diabetes Insipidus after Traumatic Brain Injury.

    PubMed

    Capatina, Cristina; Paluzzi, Alessandro; Mitchell, Rosalid; Karavitaki, Niki

    2015-07-13

    Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in many age groups. Neuroendocrine dysfunction has been recognized as a consequence of TBI and consists of both anterior and posterior pituitary insufficiency; water and electrolyte abnormalities (diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH)) are amongst the most challenging sequelae. The acute head trauma can lead (directly or indirectly) to dysfunction of the hypothalamic neurons secreting antidiuretic hormone (ADH) or of the posterior pituitary gland causing post-traumatic DI (PTDI). PTDI is usually diagnosed in the first days after the trauma presenting with hypotonic polyuria. Frequently, the poor general status of most patients prevents adequate fluid intake to compensate the losses and severe dehydration and hypernatremia occur. Management consists of careful monitoring of fluid balance and hormonal replacement. PTDI is associated with high mortality, particularly when presenting very early following the injury. In many surviving patients, the PTDI is transient, lasting a few days to a few weeks and in a minority of cases, it is permanent requiring management similar to that offered to patients with non-traumatic central DI.

  7. 78 FR 12334 - Proposed Collection; Comment Request: Federal Interagency Traumatic Brain Injury Research (FITBIR...

    Federal Register 2010, 2011, 2012, 2013, 2014

    2013-02-22

    ... Traumatic Brain Injury Research (FITBIR) Informatics System Data Access Request SUMMARY: In compliance with.... Proposed Collection: Federal Interagency Traumatic Brain Injury Research (FITBIR) Informatics System...

  8. 78 FR 37834 - Submission for OMB review; 30-Day Comment Request; Federal Interagency Traumatic Brain Injury...

    Federal Register 2010, 2011, 2012, 2013, 2014

    2013-06-24

    ... Interagency Traumatic Brain Injury Research (FITBIR) Informatics System Data Access Request SUMMARY: Under the... Collection: Federal Interagency Traumatic Brain Injury Research (FITBIR) Informatics System Data...

  9. Ulinastatin attenuates brain edema after traumatic brain injury in rats.

    PubMed

    Cui, Tao; Zhu, Gangyi

    2015-03-01

    Traumatic brain injury (TBI) remains the leading cause of injury-related death and disability. Brain edema, one of the most major complications of TBI, contributes to elevated intracranial pressure, and poor prognosis following TBI. The objective of this study was to evaluate whether Ulinastatin (UTI), a serine protease inhibitor, attenuates brain edema following TBI. Our results showed that treatment with UTI at a dose of 50,000 U/kg attenuated the brain edema, as assayed by water content 24 h after TBI induction. This attenuation was associated with a significant decrease of the expression level of aquaporin-4. In addition, we showed that UTI treatment also markedly inhibited the expression of pro-inflammatory cytokines including IL-1β and TNF-α as well as activity of NF-κB. Collectively, our findings suggested that UTI may be a promising strategy to treat brain edema following TBI.

  10. Diagnosing pseudobulbar affect in traumatic brain injury

    PubMed Central

    Engelman, William; Hammond, Flora M; Malec, James F

    2014-01-01

    Pseudobulbar affect (PBA) is defined by episodes of involuntary crying and/or laughing as a result of brain injury or other neurological disease. Epidemiology studies show that 5.3%–48.2% of people with traumatic brain injury (TBI) may have symptoms consistent with (or suggestive of) PBA. Yet it is a difficult and often overlooked condition in individuals with TBI, and is easily confused with depression or other mood disorders. As a result, it may be undertreated and persist for longer than it should. This review presents the signs and symptoms of PBA in patients with existing TBI and outlines how to distinguish PBA from other similar conditions. It also compares and contrasts the different diagnostic criteria found in the literature and briefly mentions appropriate treatments. This review follows a composite case with respect to the clinical course and treatment for PBA and presents typical challenges posed to a provider when diagnosing PBA. PMID:25336956

  11. Impaired Pituitary Axes Following Traumatic Brain Injury

    PubMed Central

    Scranton, Robert A.; Baskin, David S.

    2015-01-01

    Pituitary dysfunction following traumatic brain injury (TBI) is significant and rarely considered by clinicians. This topic has received much more attention in the last decade. The incidence of post TBI anterior pituitary dysfunction is around 30% acutely, and declines to around 20% by one year. Growth hormone and gonadotrophic hormones are the most common deficiencies seen after traumatic brain injury, but also the most likely to spontaneously recover. The majority of deficiencies present within the first year, but extreme delayed presentation has been reported. Information on posterior pituitary dysfunction is less reliable ranging from 3%–40% incidence but prospective data suggests a rate around 5%. The mechanism, risk factors, natural history, and long-term effect of treatment are poorly defined in the literature and limited by a lack of standardization. Post TBI pituitary dysfunction is an entity to recognize with significant clinical relevance. Secondary hypoadrenalism, hypothyroidism and central diabetes insipidus should be treated acutely while deficiencies in growth and gonadotrophic hormones should be initially observed. PMID:26239686

  12. Disability evaluation following traumatic brain injury.

    PubMed

    McPeak, L A; Stiers, W M; Cope, D N

    2001-08-01

    Accurate disability evaluation of a patient with TBI is a very difficult and detailed process. It requires an excellent background concerning the evaluation of all the physical, cognitive, behavioral, and functional abnormalities associated with TBI. Texts that highlight all these abnormalities include Medical Rehabilitation of Traumatic Brain Injury by Horn and Zasler and Rehabilitation of the Adult and Child with Traumatic Brain Injury by Rosenthal et al. In addition, appropriate disability rating can only be performed by a physician with expert skills in obtaining accurate historical information and completing a detailed physical examination. Often, the historical information must be obtained from many sources because the patient may supply inaccurate information because of his or her cognitive deficits. Interviews with family members, caregivers, therapists, friends, and employers are sometimes necessary to obtain an accurate historical picture. Premorbid functioning, behavior, and personality are important because previous abnormalities are often exaggerated after the TBI. The physical examination should be tailored to provide detailed objective information concerning all deficits identified through the history. If cognitive and behavioral problems are identified through either the history or examination, a neuropsychologic assessment is necessary. All this information should be available before the disability or impairment rating. Only with detailed information can a clinician provide an accurate rating.

  13. [The characteristics of blast traumatic brain injury].

    PubMed

    Matsumoto, Yoshihisa; Hatano, Ben; Matsushita, Yoshitaro; Nawashiro, Hiroshi; Shima, Katsuji

    2010-08-01

    With the increase in terrorist activity in recent times, the number of blast injuries has also increased in civilian and military settings. In a recent war, the number of patients who suffered blast traumatic brain injury (bTBI) increased, so treatment of bTBI is currently a very important issue. Blast injury is complicated and can be divided into 4 categories: primary, secondary, tertiary, and quaternary. Primary blast injury results from exposure to blast waves; secondary blast injury is trauma caused by fragments of explosive devices; tertiary blast injury is the result of collision with objects; and quaternary blast injury is the result of exposure to toxic and other substances. Blast waves mainly injure air-containing organs such as the lung, bowel, and ear. The brain may also be affected by blast waves. From the clinical perspective, hyperemia and severe cerebral edema occur frequently in patients who sustain significant bTBI. Penetrating or closed head injury caused by the explosion may be associated with vasospasm and pseudoaneurysm formation. Mild traumatic brain injury during war can be associated with posttraumatic stress disorder. To elucidate the mechanism of bTBI, many research works using animal models and computer analysis are underway. Such studies have so far shown that blast waves can cause damage to the brain tissue and cognitive deficits; however, detailed investigations on this topic are still required. Treatment of bTBI patients may require clinical knowledge and skills related to intensive care, neurology, and neurosurgery. Moreover, further research is required in this field. PMID:20697143

  14. Training to Optimize Learning after Traumatic Brain Injury

    PubMed Central

    Skidmore, Elizabeth R.

    2015-01-01

    One of the major foci of rehabilitation after traumatic brain injury is the design and implementation of interventions to train individuals to learn new knowledge and skills or new ways to access and execute previously acquired knowledge and skills. To optimize these interventions, rehabilitation professionals require a clear understanding of how traumatic brain injury impacts learning, and how specific approaches may enhance learning after traumatic brain injury. This brief conceptual review provides an overview of learning, the impact of traumatic brain injury on explicit and implicit learning, and the current state of the science examining selected training approaches designed to advance learning after traumatic brain injury. Potential directions for future scientific inquiry are discussed throughout the review. PMID:26217546

  15. Ouabain Improves Functional Recovery following Traumatic Brain Injury

    PubMed Central

    Dvela-Levitt, Moran; Ami, Hagit Cohen-Ben; Rosen, Haim; Shohami, Esther

    2014-01-01

    Abstract The cardiac steroid ouabain binds to Na+, K+-ATPase and inhibits its activity. Administration of the compound to animals and humans causes an increase in the force of contraction of heart muscle and stabilizes heart rate. In addition, this steroid promotes the growth of cardiac, vascular, and neuronal cells both in vitro and in vivo. We studied the effects of ouabain on mouse recovery following closed head injury (CHI), a model for traumatic brain injury. We show that chronic (three times a week), but not acute, intraperitoneal administration of a low dose (1 μg/kg) of ouabain significantly improves mouse recovery and functional outcome. The improvement in mouse performance was accompanied by a decrease in lesion size, estimated 43 d following the trauma. In addition, mice that underwent CHI and were treated with ouabain showed an increase in the number of proliferating cells in the subventricular zone and in the area surrounding the site of injury. Determination of the identity of the proliferating cells in the area surrounding the trauma showed that whereas there was no change in the proliferation of endothelial cells or astrocytes, neuronal cell proliferation almost doubled in the ouabain-treated mice in comparison with that of the vehicle animals. These results point to a neuroprotective effects of low doses of ouabain and imply its involvement in brain recovery and neuronal regeneration. This suggests that ouabain and maybe other cardiac steroids may be used for the treatment of traumatic brain injury. PMID:25007121

  16. Cerebral Lactate Metabolism After Traumatic Brain Injury.

    PubMed

    Patet, Camille; Suys, Tamarah; Carteron, Laurent; Oddo, Mauro

    2016-04-01

    Cerebral energy dysfunction has emerged as an important determinant of prognosis following traumatic brain injury (TBI). A number of studies using cerebral microdialysis, positron emission tomography, and jugular bulb oximetry to explore cerebral metabolism in patients with TBI have demonstrated a critical decrease in the availability of the main energy substrate of brain cells (i.e., glucose). Energy dysfunction induces adaptations of cerebral metabolism that include the utilization of alternative energy resources that the brain constitutively has, such as lactate. Two decades of experimental and human investigations have convincingly shown that lactate stands as a major actor of cerebral metabolism. Glutamate-induced activation of glycolysis stimulates lactate production from glucose in astrocytes, with subsequent lactate transfer to neurons (astrocyte-neuron lactate shuttle). Lactate is not only used as an extra energy substrate but also acts as a signaling molecule and regulator of systemic and brain glucose use in the cerebral circulation. In animal models of brain injury (e.g., TBI, stroke), supplementation with exogenous lactate exerts significant neuroprotection. Here, we summarize the main clinical studies showing the pivotal role of lactate and cerebral lactate metabolism after TBI. We also review pilot interventional studies that examined exogenous lactate supplementation in patients with TBI and found hypertonic lactate infusions had several beneficial properties on the injured brain, including decrease of brain edema, improvement of neuroenergetics via a "cerebral glucose-sparing effect," and increase of cerebral blood flow. Hypertonic lactate represents a promising area of therapeutic investigation; however, larger studies are needed to further examine mechanisms of action and impact on outcome. PMID:26898683

  17. Identification of Hematomas in Mild Traumatic Brain Injury Using an Index of Quantitative Brain Electrical Activity

    PubMed Central

    Naunheim, Rosanne; Bazarian, Jeffrey; Mould, W. Andrew; Hanley, Daniel

    2015-01-01

    Abstract Rapid identification of traumatic intracranial hematomas following closed head injury represents a significant health care need because of the potentially life-threatening risk they present. This study demonstrates the clinical utility of an index of brain electrical activity used to identify intracranial hematomas in traumatic brain injury (TBI) presenting to the emergency department (ED). Brain electrical activity was recorded from a limited montage located on the forehead of 394 closed head injured patients who were referred for CT scans as part of their standard ED assessment. A total of 116 of these patients were found to be CT positive (CT+), of which 46 patients with traumatic intracranial hematomas (CT+) were identified for study. A total of 278 patients were found to be CT negative (CT−) and were used as controls. CT scans were subjected to quanitative measurements of volume of blood and distance of bleed from recording electrodes by blinded independent experts, implementing a validated method for hematoma measurement. Using an algorithm based on brain electrical activity developed on a large independent cohort of TBI patients and controls (TBI-Index), patients were classified as either positive or negative for structural brain injury. Sensitivity to hematomas was found to be 95.7% (95% CI=85.2, 99.5), specificity was 43.9% (95% CI=38.0, 49.9). There was no significant relationship between the TBI-Index and distance of the bleed from recording sites (F=0.044, p=0.833), or volume of blood measured F=0.179, p=0.674). Results of this study are a validation and extension of previously published retrospective findings in an independent population, and provide evidence that a TBI-Index for structural brain injury is a highly sensitive measure for the detection of potentially life-threatening traumatic intracranial hematomas, and could contribute to the rapid, quantitative evaluation and treatment of such patients. PMID:25054838

  18. Biophysical mechanisms of traumatic brain injuries.

    PubMed

    Young, Lee Ann; Rule, Gregory T; Bocchieri, Robert T; Burns, Jennie M

    2015-02-01

    Despite years of effort to prevent traumatic brain injuries (TBIs), the occurrence of TBI in the United States alone has reached epidemic proportions. When an external force is applied to the head, it is converted into stresses that must be absorbed into the brain or redirected by a helmet or other protective equipment. Complex interactions of the head, neck, and jaw kinematics result in strains in the brain. Even relatively mild mechanical trauma to these tissues can initiate a neurochemical cascade that leads to TBI. Civilians and warfighters can experience head injuries in both combat and noncombat situations from a variety of threats, including ballistic and blunt impact, acceleration, and blast. It is critical to understand the physics created by these threats to develop meaningful improvements to clinical care, injury prevention, and mitigation. Here the authors review the current state of understanding of the complex loading conditions that lead to TBI and characterize how these loads are transmitted through soft tissue, the skull and into the brain, resulting in TBI. In addition, gaps in knowledge and injury thresholds are reviewed, as these must be addressed to better design strategies that reduce TBI incidence and severity. PMID:25714862

  19. Weight Drop Models in Traumatic Brain Injury.

    PubMed

    Kalish, Brian T; Whalen, Michael J

    2016-01-01

    Weight drop models in rodents have been used for several decades to advance our understanding of the pathophysiology of traumatic brain injury. Weight drop models have been used to replicate focal cerebral contusion as well as diffuse brain injury characterized by axonal damage. More recently, closed head injury models with free head rotation have been developed to model sports concussions, which feature functional disturbances in the absence of overt brain damage assessed by conventional imaging techniques. Here, we describe the history of development of closed head injury models in the first part of the chapter. In the second part, we describe the development of our own weight drop closed head injury model that features impact plus rapid downward head rotation, no structural brain injury, and long-term cognitive deficits in the case of multiple injuries. This rodent model was developed to reproduce key aspects of sports concussion so that a mechanistic understanding of how long-term cognitive deficits might develop will eventually follow. Such knowledge is hoped to impact athletes and war fighters and others who suffer concussive head injuries by leading to targeted therapies aimed at preventing cognitive and other neurological sequelae in these high-risk groups. PMID:27604720

  20. Biophysical mechanisms of traumatic brain injuries.

    PubMed

    Young, Lee Ann; Rule, Gregory T; Bocchieri, Robert T; Burns, Jennie M

    2015-02-01

    Despite years of effort to prevent traumatic brain injuries (TBIs), the occurrence of TBI in the United States alone has reached epidemic proportions. When an external force is applied to the head, it is converted into stresses that must be absorbed into the brain or redirected by a helmet or other protective equipment. Complex interactions of the head, neck, and jaw kinematics result in strains in the brain. Even relatively mild mechanical trauma to these tissues can initiate a neurochemical cascade that leads to TBI. Civilians and warfighters can experience head injuries in both combat and noncombat situations from a variety of threats, including ballistic and blunt impact, acceleration, and blast. It is critical to understand the physics created by these threats to develop meaningful improvements to clinical care, injury prevention, and mitigation. Here the authors review the current state of understanding of the complex loading conditions that lead to TBI and characterize how these loads are transmitted through soft tissue, the skull and into the brain, resulting in TBI. In addition, gaps in knowledge and injury thresholds are reviewed, as these must be addressed to better design strategies that reduce TBI incidence and severity.

  1. Imaging assessment of traumatic brain injury.

    PubMed

    Currie, Stuart; Saleem, Nayyar; Straiton, John A; Macmullen-Price, Jeremy; Warren, Daniel J; Craven, Ian J

    2016-01-01

    Traumatic brain injury (TBI) constitutes injury that occurs to the brain as a result of trauma. It should be appreciated as a heterogeneous, dynamic pathophysiological process that starts from the moment of impact and continues over time with sequelae potentially seen many years after the initial event. Primary traumatic brain lesions that may occur at the moment of impact include contusions, haematomas, parenchymal fractures and diffuse axonal injury. The presence of extra-axial intracranial lesions such as epidural and subdural haematomas and subarachnoid haemorrhage must be anticipated as they may contribute greatly to secondary brain insult by provoking brain herniation syndromes, cranial nerve deficits, oedema and ischaemia and infarction. Imaging is fundamental to the management of patients with TBI. CT remains the imaging modality of choice for initial assessment due to its ease of access, rapid acquisition and for its sensitivity for detection of acute haemorrhagic lesions for surgical intervention. MRI is typically reserved for the detection of lesions that may explain clinical symptoms that remain unresolved despite initial CT. This is especially apparent in the setting of diffuse axonal injury, which is poorly discerned on CT. Use of particular MRI sequences may increase the sensitivity of detecting such lesions: diffusion-weighted imaging defining acute infarction, susceptibility-weighted imaging affording exquisite data on microhaemorrhage. Additional advanced MRI techniques such as diffusion tensor imaging and functional MRI may provide important information regarding coexistent structural and functional brain damage. Gaining robust prognostic information for patients following TBI remains a challenge. Advanced MRI sequences are showing potential for biomarkers of disease, but this largely remains at the research level. Various global collaborative research groups have been established in an effort to combine imaging data with clinical and

  2. Imaging assessment of traumatic brain injury.

    PubMed

    Currie, Stuart; Saleem, Nayyar; Straiton, John A; Macmullen-Price, Jeremy; Warren, Daniel J; Craven, Ian J

    2016-01-01

    Traumatic brain injury (TBI) constitutes injury that occurs to the brain as a result of trauma. It should be appreciated as a heterogeneous, dynamic pathophysiological process that starts from the moment of impact and continues over time with sequelae potentially seen many years after the initial event. Primary traumatic brain lesions that may occur at the moment of impact include contusions, haematomas, parenchymal fractures and diffuse axonal injury. The presence of extra-axial intracranial lesions such as epidural and subdural haematomas and subarachnoid haemorrhage must be anticipated as they may contribute greatly to secondary brain insult by provoking brain herniation syndromes, cranial nerve deficits, oedema and ischaemia and infarction. Imaging is fundamental to the management of patients with TBI. CT remains the imaging modality of choice for initial assessment due to its ease of access, rapid acquisition and for its sensitivity for detection of acute haemorrhagic lesions for surgical intervention. MRI is typically reserved for the detection of lesions that may explain clinical symptoms that remain unresolved despite initial CT. This is especially apparent in the setting of diffuse axonal injury, which is poorly discerned on CT. Use of particular MRI sequences may increase the sensitivity of detecting such lesions: diffusion-weighted imaging defining acute infarction, susceptibility-weighted imaging affording exquisite data on microhaemorrhage. Additional advanced MRI techniques such as diffusion tensor imaging and functional MRI may provide important information regarding coexistent structural and functional brain damage. Gaining robust prognostic information for patients following TBI remains a challenge. Advanced MRI sequences are showing potential for biomarkers of disease, but this largely remains at the research level. Various global collaborative research groups have been established in an effort to combine imaging data with clinical and

  3. The Impact of Traumatic Brain Injury on the Aging Brain.

    PubMed

    Young, Jacob S; Hobbs, Jonathan G; Bailes, Julian E

    2016-09-01

    Traumatic brain injury (TBI) has come to the forefront of both the scientific and popular culture. Specifically, sports-related concussions or mild TBI (mTBI) has become the center of scientific scrutiny with a large amount of research focusing on the long-term sequela of this type of injury. As the populace continues to age, the impact of TBI on the aging brain will become clearer. Currently, reports have come to light that link TBI to neurodegenerative disorders such as Alzheimer's and Parkinson's diseases, as well as certain psychiatric diseases. Whether these associations are causations, however, is yet to be determined. Other long-term sequelae, such as chronic traumatic encephalopathy (CTE), appear to be associated with repetitive injuries. Going forward, as we gain better understanding of the pathophysiological process involved in TBI and subclinical head traumas, and individual traits that influence susceptibility to neurocognitive diseases, a clearer, more comprehensive understanding of the connection between brain injury and resultant disease processes in the aging brain will become evident. PMID:27432348

  4. Is genistein neuroprotective in traumatic brain injury?

    PubMed

    Soltani, Zahra; Khaksari, Mohammad; Jafari, Elham; Iranpour, Maryam; Shahrokhi, Nader

    2015-12-01

    The concerns about negative consequences of estrogen therapy have led to introduce other strategies to obtain estrogen's benefits in the brain. The present study tests the hypothesis that a major isoflavone of soy; genistein with estrogen-like activity can be neuroprotective in traumatic brain injury (TBI). The male Wistar rats were randomly divided to four groups: sham, TBI, vehicle and genistein. The TBI was induced by Marmarou method. The brain edema and the disruption of blood-brain-barrier (BBB) were evaluated 48 h post-TBI. Genistein (15 mg/kg) or dimethyl sulfoxide (DMSO) was injected i.p., twice after TBI. The intracranial pressure (ICP), the motor performance, and the beam-walk task (WB) were determined before trauma, on trauma day (D0), and first (D1) and second (D2) days post-TBI. Genistein inhibited a development of brain edema and a BBB permeability in TBI animals. An increase of ICP and a defect in motor and WB performance were showed following TBI, in all times evaluated. An increase of ICP induced by TBI was suppressed by genistein on D1 and D2 times. Genistein improved a motor disorder induced by TBI, on D1 and D2 times. Also an increase of traversal time in WB task was suppressed by genistein in TBI animals, on D1 and D2 times. The results of this study demonstrated that genistein can be neuroprotective in TBI. Genistein inhibited the disruption of BBB, the brain edema and the increase of ICP, and the disturbance of neurobehavioral performance in TBI. PMID:26367454

  5. Traumatic brain injury: family response and outcome.

    PubMed

    Kreutzer, J S; Marwitz, J H; Kepler, K

    1992-08-01

    Family outcome following traumatic brain injury has been the subject of investigation for nearly two decades. Researchers have reported on samples from Israel, Scotland, Denmark, England, and the United States. Cultural diversity as well as differences in design, assessment methods, injury characteristics, and definitions have contributed to difficulties establishing definitive conclusions. Findings indicate that patients' levels of emotional and personality disturbances are associated with levels of family disturbance, and are relatively more significant than physical disability. Undeniably, the long-term sequelae of injury have a long-term negative impact on families. Unfortunately, little has been done to establish the nature of family outcomes for patients younger than age 17, siblings, and less than severe injuries. Recent advances including development of valid measurement tools, definitions established through consensus, and multi-center collaborative research networks are promising and contribute to the likelihood of imminent progress.

  6. Traumatic Brain Injury Models in Animals.

    PubMed

    Rostami, Elham

    2016-01-01

    Traumatic brain injury (TBI) is the leading cause of death in young adults in industrialized nations and in the developing world the WHO considers TBI a silent epidemic caused by an increasing number of traffic accidents. Despite the major improvement of TBI outcome in the acute setting in the past 20 years, the assessment, therapeutic interventions, and prevention of long-term complications remain a challenge. In order to get a deeper insight into the pathology of TBI and advancement of medical understanding and clinical progress experimental animal models are an essential requirement. This chapter provides an overview of most commonly used experimental animal TBI models and the pathobiological findings based on current data. In addition, limitations and advantages of each TBI model are mentioned. This will hopefully give an insight into the possibilities of each model and be of value in choosing one when designing a study. PMID:27604712

  7. Inflammatory neuroprotection following traumatic brain injury.

    PubMed

    Russo, Matthew V; McGavern, Dorian B

    2016-08-19

    Traumatic brain injury (TBI) elicits an inflammatory response in the central nervous system (CNS) that involves both resident and peripheral immune cells. Neuroinflammation can persist for years following a single TBI and may contribute to neurodegeneration. However, administration of anti-inflammatory drugs shortly after injury was not effective in the treatment of TBI patients. Some components of the neuroinflammatory response seem to play a beneficial role in the acute phase of TBI. Indeed, following CNS injury, early inflammation can set the stage for proper tissue regeneration and recovery, which can, perhaps, explain why general immunosuppression in TBI patients is disadvantageous. Here, we discuss some positive attributes of neuroinflammation and propose that inflammation be therapeutically guided in TBI patients rather than globally suppressed. PMID:27540166

  8. Animal models of traumatic brain injury

    PubMed Central

    Xiong, Ye; Mahmood, Asim; Chopp, Michael

    2014-01-01

    Traumatic brain injury (TBI) is a leading cause of mortality and morbidity in both civilian life and the battlefield worldwide. Survivors of TBI frequently experience long-term disabling changes in cognition, sensorimotor function and personality. Over the past three decades, animal models have been developed to replicate the various aspects of human TBI, to better understand the underlying pathophysiology and to explore potential treatments. Nevertheless, promising neuroprotective drugs, which were identified to be effective in animal TBI models, have all failed in phase II or phase III clinical trials. This failure in clinical translation of preclinical studies highlights a compelling need to revisit the current status of animal models of TBI and therapeutic strategies. PMID:23329160

  9. Neuropathology of explosive blast traumatic brain injury.

    PubMed

    Magnuson, John; Leonessa, Fabio; Ling, Geoffrey S F

    2012-10-01

    During the conflicts of the Global War on Terror, which are Operation Enduring Freedom (OEF) in Afghanistan and Operation Iraqi Freedom (OIF), there have been over a quarter of a million diagnosed cases of traumatic brain injury (TBI). The vast majority are due to explosive blast. Although explosive blast TBI (bTBI) shares many clinical features with closed head TBI (cTBI) and penetrating TBI (pTBI), it has unique features, such as early cerebral edema and prolonged cerebral vasospasm. Evolving work suggests that diffuse axonal injury (DAI) seen following explosive blast exposure is different than DAI from focal impact injury. These unique features support the notion that bTBI is a separate and distinct form of TBI. This review summarizes the current state of knowledge pertaining to bTBI. Areas of discussion are: the physics of explosive blast generation, blast wave interaction with the bony calvarium and brain tissue, gross tissue pathophysiology, regional brain injury, and cellular and molecular mechanisms of explosive blast neurotrauma.

  10. Decompressive craniectomy following traumatic brain injury: developing the evidence base

    PubMed Central

    Kolias, Angelos G.; Adams, Hadie; Timofeev, Ivan; Czosnyka, Marek; Corteen, Elizabeth A.; Pickard, John D.; Turner, Carole; Gregson, Barbara A.; Kirkpatrick, Peter J.; Murray, Gordon D.; Menon, David K.; Hutchinson, Peter J.

    2016-01-01

    Abstract In the context of traumatic brain injury (TBI), decompressive craniectomy (DC) is used as part of tiered therapeutic protocols for patients with intracranial hypertension (secondary or protocol-driven DC). In addition, the bone flap can be left out when evacuating a mass lesion, usually an acute subdural haematoma (ASDH), in the acute phase (primary DC). Even though, the principle of “opening the skull” in order to control brain oedema and raised intracranial pressure has been practised since the beginning of the 20th century, the last 20 years have been marked by efforts to develop the evidence base with the conduct of randomised trials. This article discusses the merits and challenges of this approach and provides an overview of randomised trials of DC following TBI. An update on the RESCUEicp study, a randomised trial of DC versus advanced medical management (including barbiturates) for severe and refractory post-traumatic intracranial hypertension is provided. In addition, the rationale for the RESCUE-ASDH study, the first randomised trial of primary DC versus craniotomy for adult head-injured patients with an ASDH, is presented. PMID:26972805

  11. Strategic Learning in Youth with Traumatic Brain Injury: Evidence for Stall in Higher-Order Cognition

    ERIC Educational Resources Information Center

    Gamino, Jacquelyn F.; Chapman, Sandra B.; Cook, Lori G.

    2009-01-01

    Little is known about strategic learning ability in preteens and adolescents with traumatic brain injury (TBI). Strategic learning is the ability to combine and synthesize details to form abstracted gist-based meanings, a higher-order cognitive skill associated with frontal lobe functions and higher classroom performance. Summarization tasks were…

  12. Classroom Strategies for Teaching Veterans with Post-Traumatic Stress Disorder and Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Sinski, Jennifer Blevins

    2012-01-01

    Postsecondary institutions currently face the largest influx of veteran students since World War II. As the number of veteran students who may experience learning problems caused by Post-Traumatic Stress Disorder and/or Traumatic Brain Injury continues to rise, the need for instructional strategies that address their needs increases. Educators may…

  13. The Effects of Mild Traumatic Brain Injury, Post-Traumatic Stress Disorder, and Combined Mild Traumatic Brain Injury/Post-Traumatic Stress Disorder on Returning Veterans

    PubMed Central

    Combs, Hannah L.; Berry, David T. R.; Pape, Theresa; Babcock-Parziale, Judith; Smith, Bridget; Schleenbaker, Randal; Shandera-Ochsner, Anne; Harp, Jordan P.

    2015-01-01

    Abstract United States veterans of the Iraqi (Operation Iraqi Freedom [OIF]) and Afghanistan (Operation Enduring Freedom [OEF]) conflicts have frequently returned from deployment after sustaining mild traumatic brain injury (mTBI) and enduring stressful events resulting in post-traumatic stress disorder (PTSD). A large number of returning service members have been diagnosed with both a history of mTBI and current PTSD. Substantial literature exists on the neuropsychological factors associated with mTBI and PTSD occurring separately; far less research has explored the combined effects of PTSD and mTBI. The current study employed neuropsychological and psychological measures in a sample of 251 OIF/OEF veterans to determine whether participants with a history of mTBI and current PTSD (mTBI+PTSD) have poorer cognitive and psychological outcomes than participants with mTBI only (mTBI-o), PTSD only (PTSD-o), or veteran controls (VC), when groups are comparable on intelligence quotient, education, and age. The mTBI+PTSD group performed more poorly than VC, mTBI-o, and PTSD-o groups on several neuropsychological measures. Effect size comparisons suggest small deleterious effects for mTBI-o on measures of processing speed and visual attention and small effects for PTSD-o on measures of verbal memory, with moderate effects for mTBI+PTSD on the same variables. Additionally, the mTBI+PTSD group was significantly more psychologically distressed than the PTSD-o group, and PTSD-o group was more distressed than VC and mTBI-o groups. These findings suggest that veterans with mTBI+PTSD perform significantly lower on neuropsychological and psychiatric measures than veterans with mTBI-o or PTSD-o. The results also raise the possibility of mild but persisting cognitive changes following mTBI sustained during deployment. PMID:25350012

  14. Critical care management of severe traumatic brain injury in adults

    PubMed Central

    2012-01-01

    Traumatic brain injury (TBI) is a major medical and socio-economic problem, and is the leading cause of death in children and young adults. The critical care management of severe TBI is largely derived from the "Guidelines for the Management of Severe Traumatic Brain Injury" that have been published by the Brain Trauma Foundation. The main objectives are prevention and treatment of intracranial hypertension and secondary brain insults, preservation of cerebral perfusion pressure (CPP), and optimization of cerebral oxygenation. In this review, the critical care management of severe TBI will be discussed with focus on monitoring, avoidance and minimization of secondary brain insults, and optimization of cerebral oxygenation and CPP. PMID:22304785

  15. The gut reaction to traumatic brain injury

    PubMed Central

    Katzenberger, Rebeccah J; Ganetzky, Barry; Wassarman, David A

    2015-01-01

    Traumatic brain injury (TBI) is a complex disorder that affects millions of people worldwide. The complexity of TBI partly stems from the fact that injuries to the brain instigate non-neurological injuries to other organs such as the intestine. Additionally, genetic variation is thought to play a large role in determining the nature and severity of non-neurological injuries. We recently reported that TBI in flies, as in humans, increases permeability of the intestinal epithelial barrier resulting in hyperglycemia and a higher risk of death. Furthermore, we demonstrated that genetic variation in flies is also pertinent to the complexity of non-neurological injuries following TBI. The goals of this review are to place our findings in the context of what is known about TBI-induced intestinal permeability from studies of TBI patients and rodent TBI models and to draw attention to how studies of the fly TBI model can provide unique insights that may facilitate diagnosis and treatment of TBI. PMID:26291482

  16. Outcome measures for traumatic brain injury.

    PubMed

    Shukla, Dhaval; Devi, B Indira; Agrawal, Amit

    2011-07-01

    Traumatic brain injury (TBI) is a major public health problem resulting in death and disabilities of young and productive people. Though the mortality of TBI has decreased substantially in recent years the disability due to TBI has not appreciably reduced. Various outcome scales have been proposed and used to assess disability after TBI. A few, commonly used are Glasgow Outcome Scale (GOS) with or without extended scores, Disability Rating Scale (DRS), Functional Independence Measure (FIM), Community Integration Questionnaire (CIQ), and the Functional Status Examination (FSE). These scales assess disability resulting from physical and cognitive impairments. For patients with good physical recovery a cognitive and neuropsychological outcome measure is required. Such measures include Neurobehavioural Function Inventory and specific neuropsychological tests like Rey Complex Figure for visuoconstruction and memory, Controlled Oral Word Association for verbal fluency, Symbol Digit Modalities (verbal) for sustained attention and Grooved Pegboard for fine motor dexterity. A more holistic and complete outcome measure is Quality of Life (QOL). Disease specific QOL measure for TBI, Quality of Life after Brain Injury (QOLIBRI) has also been recently proposed. The problems with outcome measures include poor operational definitions, lack of sensitivity or low ceiling effects, inability to evaluate patients who cannot report, lack of integration of morbidity and mortality categories, and limited domains of functioning assessed. GOSE-E satisfies most of the criteria of good outcome scale and in combination with neuropsychological tests is a near complete instrument for assessment of outcome after TBI. PMID:21440363

  17. Emerging Therapies in Traumatic Brain Injury

    PubMed Central

    Kochanek, Patrick M.; Jackson, Travis C.; Ferguson, Nikki Miller; Carlson, Shaun W.; Simon, Dennis W.; Brockman, Erik C.; Ji, Jing; Bayir, Hülya; Poloyac, Samuel M.; Wagner, Amy K.; Kline, Anthony E.; Empey, Philip E.; Clark, Robert S.B.; Jackson, Edwin K.; Dixon, C. Edward

    2015-01-01

    Despite decades of basic and clinical research, treatments to improve outcomes after traumatic brain injury (TBI) are limited. However, based on the recent recognition of the prevalence of mild TBI, and its potential link to neurodegenerative disease, many new and exciting secondary injury mechanisms have been identified and several new therapies are being evaluated targeting both classic and novel paradigms. This includes a robust increase in both preclinical and clinical investigations. Using a mechanism-based approach the authors define the targets and emerging therapies for TBI. They address putative new therapies for TBI across both the spectrum of injury severity and the continuum of care, from the field to rehabilitation. They discuss TBI therapy using 11 categories, namely, (1) excitotoxicity and neuronal death, (2) brain edema, (3) mitochondria and oxidative stress, (4) axonal injury, (5) inflammation, (6) ischemia and cerebral blood flow dysregulation, (7) cognitive enhancement, (8) augmentation of endogenous neuroprotection, (9) cellular therapies, (10) combination therapy, and (11) TBI resuscitation. The current golden age of TBI research represents a special opportunity for the development of breakthroughs in the field. PMID:25714870

  18. ANTIOXIDANT THERAPIES FOR TRAUMATIC BRAIN INJURY

    PubMed Central

    Hall, Edward D.; Vaishnav, Radhika A.; Mustafa, Ayman G.

    2010-01-01

    Free radical-induced oxidative damage reactions, and membrane lipid peroxidation (LP) in particular, are one of the best validated secondary injury mechanisms in preclinical traumatic brain injury models. In addition to the disruption of the membrane phospholipid architecture, LP results in the formation of cytotoxic aldehyde-containing products that bind to cellular proteins and impair their normal functions. This article reviews the progress over the past three decades in regards to the preclinical discovery and attempted clinical development of antioxidant drugs designed to inhibit free radical-induced LP and its neurotoxic consequences via different mechanisms including the O2•- scavenger superoxide dismutase (SOD) and the lipid peroxidation inhibitor tirilazad. In addition, various other antioxidant agents that have been shown to have efficacy in preclinical TBI models are briefly presented such as the LP inhibitors U83836E, resveratrol, curcumin, OPC-14177 and lipoic acid; the iron chelator deferoxamine and the nitroxide-containing antioxidants such as α-phenyl-tert-butyl nitrone and tempol. A relatively new antioxidant mechanistic strategy for acute TBI is aimed at the scavenging of aldehydic LP by-products that are highly neurotoxic with “carbonyl scavenging” compounds. Finally, it is proposed that the most effective approach to interrupt posttraumatic oxidative brain damage after TBI might involve the combined treatment with mechanistically-complementary antioxidants that simultaneously scavenge LP-initiating free radicals, inhibit LP propagation and lastly remove neurotoxic LP byproducts. PMID:20129497

  19. Military-related traumatic brain injury and neurodegeneration.

    PubMed

    McKee, Ann C; Robinson, Meghan E

    2014-06-01

    Mild traumatic brain injury (mTBI) includes concussion, subconcussion, and most exposures to explosive blast from improvised explosive devices. mTBI is the most common traumatic brain injury affecting military personnel; however, it is the most difficult to diagnose and the least well understood. It is also recognized that some mTBIs have persistent, and sometimes progressive, long-term debilitating effects. Increasing evidence suggests that a single traumatic brain injury can produce long-term gray and white matter atrophy, precipitate or accelerate age-related neurodegeneration, and increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease. In addition, repetitive mTBIs can provoke the development of a tauopathy, chronic traumatic encephalopathy. We found early changes of chronic traumatic encephalopathy in four young veterans of the Iraq and Afghanistan conflict who were exposed to explosive blast and in another young veteran who was repetitively concussed. Four of the five veterans with early-stage chronic traumatic encephalopathy were also diagnosed with posttraumatic stress disorder. Advanced chronic traumatic encephalopathy has been found in veterans who experienced repetitive neurotrauma while in service and in others who were accomplished athletes. Clinically, chronic traumatic encephalopathy is associated with behavioral changes, executive dysfunction, memory loss, and cognitive impairments that begin insidiously and progress slowly over decades. Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus; septal abnormalities; and abnormal deposits of hyperphosphorylated tau as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy has clinical and

  20. Military-related traumatic brain injury and neurodegeneration

    PubMed Central

    McKee, Ann C.; Robinson, Meghan E.

    2014-01-01

    Mild traumatic brain injury (mTBI) includes concussion, subconcussion, and most exposures to explosive blast from improvised explosive devices. mTBI is the most common traumatic brain injury affecting military personnel; however, it is the most difficult to diagnose and the least well understood. It is also recognized that some mTBIs have persistent, and sometimes progressive, long-term debilitating effects. Increasing evidence suggests that a single traumatic brain injury can produce long-term gray and white matter atrophy, precipitate or accelerate age-related neurodegeneration, and increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease. In addition, repetitive mTBIs can provoke the development of a tauopathy, chronic traumatic encephalopathy. We found early changes of chronic traumatic encephalopathy in four young veterans of the Iraq and Afghanistan conflict who were exposed to explosive blast and in another young veteran who was repetitively concussed. Four of the five veterans with early-stage chronic traumatic encephalopathy were also diagnosed with posttraumatic stress disorder. Advanced chronic traumatic encephalopathy has been found in veterans who experienced repetitive neurotrauma while in service and in others who were accomplished athletes. Clinically, chronic traumatic encephalopathy is associated with behavioral changes, executive dysfunction, memory loss, and cognitive impairments that begin insidiously and progress slowly over decades. Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus; septal abnormalities; and abnormal deposits of hyperphosphorylated tau as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy has clinical and

  1. Dementia Resulting From Traumatic Brain Injury

    PubMed Central

    Shively, Sharon; Scher, Ann I.; Perl, Daniel P.; Diaz-Arrastia, Ramon

    2013-01-01

    Traumatic brain injury (TBI) is among the earliest illnesses described in human history and remains a major source of morbidity and mortality in the modern era. It is estimated that 2% of the US population lives with long-term disabilities due to a prior TBI, and incidence and prevalence rates are even higher in developing countries. One of the most feared long-term consequences of TBIs is dementia, as multiple epidemiologic studies show that experiencing a TBI in early or midlife is associated with an increased risk of dementia in late life. The best data indicate that moderate and severe TBIs increase risk of dementia between 2-and 4-fold. It is less clear whether mild TBIs such as brief concussions result in increased dementia risk, in part because mild head injuries are often not well documented and retrospective studies have recall bias. However, it has been observed for many years that multiple mild TBIs as experienced by professional boxers are associated with a high risk of chronic traumatic encephalopathy (CTE), a type of dementia with distinctive clinical and pathologic features. The recent recognition that CTE is common in retired professional football and hockey players has rekindled interest in this condition, as has the recognition that military personnel also experience high rates of mild TBIs and may have a similar syndrome. It is presently unknown whether dementia in TBI survivors is pathophysiologically similar to Alzheimer disease, CTE, or some other entity. Such information is critical for developing preventive and treatment strategies for a common cause of acquired dementia. Herein, we will review the epidemiologic data linking TBI and dementia, existing clinical and pathologic data, and will identify areas where future research is needed. PMID:22776913

  2. What Can I Do to Help Prevent Traumatic Brain Injury?

    MedlinePlus

    ... to Congress: Epidemiology and Rehabilitation Report to Congress: Military Personnel TBI in the US: Emergency Department Visits, Hospitalizations ... sustaining a traumatic brain injury, including: Buckling your child in the car using a child safety seat, ...

  3. How Do Health Care Providers Diagnose Traumatic Brain Injury (TBI)?

    MedlinePlus

    ... Information Clinical Trials Resources and Publications How do health care providers diagnose traumatic brain injury (TBI)? Skip sharing ... links Share this: Page Content To diagnose TBI, health care providers may use one or more tests that ...

  4. Role of Metabolomics in Traumatic Brain Injury Research.

    PubMed

    Wolahan, Stephanie M; Hirt, Daniel; Braas, Daniel; Glenn, Thomas C

    2016-10-01

    Metabolomics is an important member of the omics community in that it defines which small molecules may be responsible for disease states. This article reviews the essential principles of metabolomics from specimen preparation, chemical analysis, to advanced statistical methods. Metabolomics in traumatic brain injury has so far been underutilized. Future metabolomics-based studies focused on the diagnoses, prognoses, and treatment effects need to be conducted across all types of traumatic brain injury. PMID:27637396

  5. Structural and functional connectivity in traumatic brain injury

    PubMed Central

    Xiao, Hui; Yang, Yang; Xi, Ji-hui; Chen, Zi-qian

    2015-01-01

    Traumatic brain injury survivors often experience cognitive deficits and neuropsychiatric symptoms. However, the neurobiological mechanisms underlying specific impairments are not fully understood. Advances in neuroimaging techniques (such as diffusion tensor imaging and functional MRI) have given us new insights on structural and functional connectivity patterns of the human brain in both health and disease. The connectome derived from connectivity maps reflects the entire constellation of distributed brain networks. Using these powerful neuroimaging approaches, changes at the microstructural level can be detected through regional and global properties of neuronal networks. Here we will review recent developments in the study of brain network abnormalities in traumatic brain injury, mainly focusing on structural and functional connectivity. Some connectomic studies have provided interesting insights into the neurological dysfunction that occurs following traumatic brain injury. These techniques could eventually be helpful in developing imaging biomarkers of cognitive and neurobehavioral sequelae, as well as predicting outcome and prognosis. PMID:26889200

  6. [Anti-inflammatory modulators in traumatic brain injury].

    PubMed

    Lescot, T; Marchand-Verrecchia, C; Puybasset, L

    2006-07-01

    Traumatic brain injury leads to primary and secondary brain injuries. Primary brain injury results from mechanical forces applied to the head at the time of impact. Secondary brain injury occurs at some time after the primary impact. Numerous pathophysiological mechanisms have been postulated to explain the progressive tissue damage produced by secondary injuries. The endogenous neuroinflammatory response after traumatic brain injury contributes to the development of blood-brain barrier breakdown, cerebral oedema and neuronal cell death and this has led to various pharmacological therapies to try to limit this type of damage. Studies employing glutamate receptor antagonist for cerebral protection have yielded promising results in laboratory animals but failed to produce clinically significant improvements. The present review will summarize the mechanisms of post traumatic cerebral inflammation with a special focus on the anti-inflammatory drug targets.

  7. Classification of Traumatic Brain Injury for Targeted Therapies

    PubMed Central

    Saatman, Kathryn E.; Duhaime, Ann-Christine; Bullock, Ross; Maas, Andrew I.R.; Valadka, Alex

    2008-01-01

    Abstract The heterogeneity of traumatic brain injury (TBI) is considered one of the most significant barriers to finding effective therapeutic interventions. In October, 2007, the National Institute of Neurological Disorders and Stroke, with support from the Brain Injury Association of America, the Defense and Veterans Brain Injury Center, and the National Institute of Disability and Rehabilitation Research, convened a workshop to outline the steps needed to develop a reliable, efficient and valid classification system for TBI that could be used to link specific patterns of brain and neurovascular injury with appropriate therapeutic interventions. Currently, the Glasgow Coma Scale (GCS) is the primary selection criterion for inclusion in most TBI clinical trials. While the GCS is extremely useful in the clinical management and prognosis of TBI, it does not provide specific information about the pathophysiologic mechanisms which are responsible for neurological deficits and targeted by interventions. On the premise that brain injuries with similar pathoanatomic features are likely to share common pathophysiologic mechanisms, participants proposed that a new, multidimensional classification system should be developed for TBI clinical trials. It was agreed that preclinical models were vital in establishing pathophysiologic mechanisms relevant to specific pathoanatomic types of TBI and verifying that a given therapeutic approach improves outcome in these targeted TBI types. In a clinical trial, patients with the targeted pathoanatomic injury type would be selected using an initial diagnostic entry criterion, including their severity of injury. Coexisting brain injury types would be identified and multivariate prognostic modeling used for refinement of inclusion/exclusion criteria and patient stratification. Outcome assessment would utilize endpoints relevant to the targeted injury type. Advantages and disadvantages of currently available diagnostic, monitoring, and

  8. An update on traumatic brain injuries.

    PubMed

    Timmons, S D

    2012-09-01

    Severe traumatic brain injury (TBI) represents a major cause of neurological mortality and morbidity throughout the world. Several challenges have been faced in the conduct of clinical research in TBI in past decades, including inclusion of a broad heterogeneity of injuries, difficulties with standardization and consistency of complex medical management, and lack of sophisticated outcomes measures to sufficiently detect differences in outcomes. Consequently, evidence-based guidelines for targeted therapeutic approaches remain for the most part at the level of Class II or III evidence. Harnessing the power of computing is paramount to our understanding of different prognostic groups in order to devise treatments of the future. Multimodality bedside monitoring of various physiological parameters and events can be deployed in the intensive care unit (ICU) but better data repositories and analytics are required. Recent developments in neuroimaging and definition of potential genetic and biological markers in TBI are also aiding in the sub-categorization of patients into finer diagnostic and prognostic groups. Using mathematical prediction models incorporating the plethora of data gathered, future research will provide means of tailoring therapies to individuals based upon best evidence in populations similar to them, and according to their own biological and physiological situation.

  9. Iatrogenic traumatic brain injury during tooth extraction.

    PubMed

    Troxel, Mark

    2015-01-01

    An 8 yr old spayed female Yorkshire terrier was referred for evaluation of progressive neurological signs after a routine dental prophylaxis with tooth extractions. The patient was circling to the left and blind in the right eye with right hemiparesis. Neurolocalization was to the left forebrain. MRI revealed a linear tract extending from the caudal oropharynx, through the left retrobulbar space and frontal lobe, into the left parietal lobe. A small skull fracture was identified in the frontal bone through which the linear tract passed. Those findings were consistent with iatrogenic trauma from slippage of a dental elevator during extraction of tooth 210. The dog was treated empirically with clindamycin. The patient regained most of its normal neurological function within the first 4 mo after the initial injury. Although still not normal, the dog has a good quality of life. Traumatic brain injury is a rarely reported complication of extraction. Care must be taken while performing dental cleaning and tooth extraction, especially of the maxillary premolar and molar teeth to avoid iatrogenic damage to surrounding structures.

  10. Advanced Neuroimaging in Traumatic Brain Injury

    PubMed Central

    Edlow, Brian L.; Wu, Ona

    2013-01-01

    Advances in structural and functional neuroimaging have occurred at a rapid pace over the past two decades. Novel techniques for measuring cerebral blood flow, metabolism, white matter connectivity, and neural network activation have great potential to improve the accuracy of diagnosis and prognosis for patients with traumatic brain injury (TBI), while also providing biomarkers to guide the development of new therapies. Several of these advanced imaging modalities are currently being implemented into clinical practice, whereas others require further development and validation. Ultimately, for advanced neuroimaging techniques to reach their full potential and improve clinical care for the many civilians and military personnel affected by TBI, it is critical for clinicians to understand the applications and methodological limitations of each technique. In this review, we examine recent advances in structural and functional neuroimaging and the potential applications of these techniques to the clinical care of patients with TBI. We also discuss pitfalls and confounders that should be considered when interpreting data from each technique. Finally, given the vast amounts of advanced imaging data that will soon be available to clinicians, we discuss strategies for optimizing data integration, visualization and interpretation. PMID:23361483

  11. Iatrogenic traumatic brain injury during tooth extraction.

    PubMed

    Troxel, Mark

    2015-01-01

    An 8 yr old spayed female Yorkshire terrier was referred for evaluation of progressive neurological signs after a routine dental prophylaxis with tooth extractions. The patient was circling to the left and blind in the right eye with right hemiparesis. Neurolocalization was to the left forebrain. MRI revealed a linear tract extending from the caudal oropharynx, through the left retrobulbar space and frontal lobe, into the left parietal lobe. A small skull fracture was identified in the frontal bone through which the linear tract passed. Those findings were consistent with iatrogenic trauma from slippage of a dental elevator during extraction of tooth 210. The dog was treated empirically with clindamycin. The patient regained most of its normal neurological function within the first 4 mo after the initial injury. Although still not normal, the dog has a good quality of life. Traumatic brain injury is a rarely reported complication of extraction. Care must be taken while performing dental cleaning and tooth extraction, especially of the maxillary premolar and molar teeth to avoid iatrogenic damage to surrounding structures. PMID:25695556

  12. Persuasive Discourse Impairments in Traumatic Brain Injury

    PubMed Central

    Ghayoumi, Zahra; Yadegari, Fariba; Mahmoodi-Bakhtiari, Behrooz; Fakharian, Esmaeil; Rahgozar, Mehdi; Rasouli, Maryam

    2015-01-01

    Background: Considering the cognitive and linguistic complexity of discourse production, it is expected that individuals with traumatic brain injury (TBI) should face difficulties in this task. Therefore, clinical examination of discourse has become a useful tool for studying and assessment of communication skills of people suffering from TBI. Among different genres of discourse, persuasive discourse is considered as a more cognitively demanding task. However, little is known about persuasive discourse in individuals suffering from TBI. Objectives: The purpose of this study was to evaluate the performance of adults with TBI on a task of spoken persuasive discourse to determine the impaired linguistic measures. Patients and Methods: Thirteen TBI nonaphasic Persian speaking individuals, ranged between 19 to 40 years (Mean = 25.64 years; SD = 6.10) and 59 healthy adults matched by age, were asked to perform the persuasive discourse task. The task included asking the participants to express their opinion on a topic, and after the analysis of the produced discourse, the two groups were compared on the basis of their language productivity, sentential complexity, maze ratio and cohesion ratio. Results: The TBI group produced discourses with less productivity, sentential complexity, cohesion ratio and more maze ratio compared the control group. Conclusions: As it is important to consider acquired communication disorders particularly discourse impairment of brain injured patients along with their other clinical impairments and regarding the fact that persuasive discourse is crucial in academic and social situations, the persuasive discourse task presented in this study could be a useful tool for speech therapists, intending to evaluate communication disorders in patients with TBI. PMID:25798418

  13. Intravenous Fluid Therapy in Traumatic Brain Injury and Decompressive Craniectomy

    PubMed Central

    Alvis-Miranda, Hernando Raphael; Castellar-Leones, Sandra Milena; Moscote-Salazar, Luis Rafael

    2014-01-01

    The patient with head trauma is a challenge for the emergency physician and for the neurosurgeon. Currently traumatic brain injury constitutes a public health problem. Knowledge of the various supportive therapeutic strategies in the pre-hospital and pre-operative stages is essential for optimal care. The immediate rapid infusion of large volumes of crystalloids to restore blood volume and blood pressure is now the standard treatment of patients with combined traumatic brain injury (TBI) and hemorrhagic shock (HS). The fluid in patients with brain trauma and especially in patients with brain injur y is a critical issue. In this context we present a review of the literature about the history, physiology of current fluid preparations, and a discussion regarding the use of fluid therapy in traumatic brain injury and decompressive craniectomy. PMID:27162857

  14. Combat-related headache and traumatic brain injury.

    PubMed

    Waung, Maggie W; Abrams, Gary M

    2012-12-01

    Post-traumatic headache is a commonly described complication of traumatic brain injury. Recent studies highlight differences between headache features of combat veterans who suffered traumatic brain injury compared to civilians. Not surprisingly, there is a higher rate of associated PTSD and sleep disturbances among veterans. Factors of lower socioeconomic status, rank, and multiple head injuries appear to have a similar effect on post-traumatic headache in combat-related traumatic brain injury. Areas of discordance in the literature include the effect of prolonged loss of consciousness and the prevalence of specific headache phenotypes following head trauma. To date, there have been no randomized trials of treatment for post-traumatic headache. This may be related to the variability of headache features and uncertainty of pathophysiologic mechanisms. Given this lack of data, many practitioners follow treatment guidelines for primary headaches. Additionally, because of mounting data linking PTSD to post-traumatic headache in combat veterans, it may be crucial to choose multimodal agents and take a multidisciplinary approach to combat-related headache.

  15. Cell-Based therapy for traumatic brain injury

    PubMed Central

    Gennai, S.; Monsel, A.; Hao, Q.; Liu, J.; Gudapati, V.; Barbier, E. L.; Lee, J. W.

    2015-01-01

    Traumatic brain injury is a major economic burden to hospitals in terms of emergency department visits, hospitalizations, and utilization of intensive care units. Current guidelines for the management of severe traumatic brain injuries are primarily supportive, with an emphasis on surveillance (i.e. intracranial pressure) and preventive measures to reduce morbidity and mortality. There are no direct effective therapies available. Over the last fifteen years, pre-clinical studies in regenerative medicine utilizing cell-based therapy have generated enthusiasm as a possible treatment option for traumatic brain injury. In these studies, stem cells and progenitor cells were shown to migrate into the injured brain and proliferate, exerting protective effects through possible cell replacement, gene and protein transfer, and release of anti-inflammatory and growth factors. In this work, we reviewed the pathophysiological mechanisms of traumatic brain injury, the biological rationale for using stem cells and progenitor cells, and the results of clinical trials using cell-based therapy for traumatic brain injury. Although the benefits of cell-based therapy have been clearly demonstrated in pre-clinical studies, some questions remain regarding the biological mechanisms of repair and safety, dose, route and timing of cell delivery, which ultimately will determine its optimal clinical use. PMID:26170348

  16. Graph Analysis of Functional Brain Networks for Cognitive Control of Action in Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Caeyenberghs, Karen; Leemans, Alexander; Heitger, Marcus H.; Leunissen, Inge; Dhollander, Thijs; Sunaert, Stefan; Dupont, Patrick; Swinnen, Stephan P.

    2012-01-01

    Patients with traumatic brain injury show clear impairments in behavioural flexibility and inhibition that often persist beyond the time of injury, affecting independent living and psychosocial functioning. Functional magnetic resonance imaging studies have shown that patients with traumatic brain injury typically show increased and more broadly…

  17. Exercise to enhance neurocognitive function after traumatic brain injury.

    PubMed

    Fogelman, David; Zafonte, Ross

    2012-11-01

    Vigorous exercise has long been associated with improved health in many domains. Results of clinical observation have suggested that neurocognitive performance also is improved by vigorous exercise. Data derived from animal model-based research have been emerging that show molecular and neuroanatomic mechanisms that may explain how exercise improves cognition, particularly after traumatic brain injury. This article will summarize the current state of the basic science and clinical literature regarding exercise as an intervention, both independently and in conjunction with other modalities, for brain injury rehabilitation. A key principle is the factor of timing of the initiation of exercise after mild traumatic brain injury, balancing potentially favorable and detrimental effects on recovery.

  18. Neurotherapy of Traumatic Brain Injury/Post-Traumatic Stress Symptoms in Vietnam Veterans.

    PubMed

    Nelson, David V; Esty, Mary Lee

    2015-10-01

    Previous report suggested the beneficial effects of an adaptation of the Flexyx Neurotherapy System (FNS) for the amelioration of mixed traumatic brain injury/post-traumatic stress symptoms in veterans of the Afghanistan and Iraq wars. As a novel variant of electroencephalograph biofeedback, FNS falls within the bioenergy domain of complementary and alternative medicine. Rather than learning voluntary control over the production/inhibition of brain wave patterns, FNS involves offsetting stimulation of brain wave activity by means of an external energy source, specifically, the conduction of electromagnetic energy stimulation via the connecting electroencephalograph cables. Essentially, these procedures subliminally induce strategic distortion of ongoing brain wave activity to presumably facilitate resetting of more adaptive patterns of activity. Reported herein are two cases of Vietnam veterans with mixed traumatic brain injury/post-traumatic stress symptoms, each treated with FNS for 25 sessions. Comparisons of pre- and post-treatment questionnaire assessments revealed notable decreases for all symptoms, suggesting improvements across the broad domains of cognition, pain, sleep, fatigue, and mood/emotion, including post-traumatic stress symptoms, as well as for overall activity levels. Findings suggest FNS treatment may be of potential benefit for the partial amelioration of symptoms, even in some individuals for whom symptoms have been present for decades.

  19. Neuropsychological Consequences of Traumatic Brain Injury in Children and Adolescents.

    ERIC Educational Resources Information Center

    Lord-Maes, Janiece; Obrzut, John E.

    1996-01-01

    This article discusses recent findings concerning cognitive outcomes in traumatic brain injury (TBI) in children and adolescents, with a particular focus on age differences with TBI. It suggests a relationship between specific learning disorders and brain dysfunction, addresses differential hemispheric functioning with TBI, and outlines recent…

  20. White Matter Damage and Cognitive Impairment after Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Kinnunen, Kirsi Maria; Greenwood, Richard; Powell, Jane Hilary; Leech, Robert; Hawkins, Peter Charlie; Bonnelle, Valerie; Patel, Maneesh Chandrakant; Counsell, Serena Jane; Sharp, David James

    2011-01-01

    White matter disruption is an important determinant of cognitive impairment after brain injury, but conventional neuroimaging underestimates its extent. In contrast, diffusion tensor imaging provides a validated and sensitive way of identifying the impact of axonal injury. The relationship between cognitive impairment after traumatic brain injury…

  1. Aging, Neurodegenerative Disease, and Traumatic Brain Injury: The Role of Neuroimaging

    PubMed Central

    Levine, Brian

    2015-01-01

    Abstract Traumatic brain injury (TBI) is a highly prevalent condition with significant effects on cognition and behavior. While the acute and sub-acute effects of TBI recover over time, relatively little is known about the long-term effects of TBI in relation to neurodegenerative disease. This issue has recently garnered a great deal of attention due to publicity surrounding chronic traumatic encephalopathy (CTE) in professional athletes, although CTE is but one of several neurodegenerative disorders associated with a history of TBI. Here, we review the literative on neurodegenerative disorders linked to remote TBI. We also review the evidence for neuroimaging changes associated with unhealthy brain aging in the context of remote TBI. We conclude that neuroimaging biomarkers have significant potential to increase understanding of the mechanisms of unhealthy brain aging and neurodegeneration following TBI, with potential for identifying those at risk for unhealthy brain aging prior to the clinical manifestation of neurodegenerative disease. PMID:25192426

  2. Robust whole-brain segmentation: application to traumatic brain injury.

    PubMed

    Ledig, Christian; Heckemann, Rolf A; Hammers, Alexander; Lopez, Juan Carlos; Newcombe, Virginia F J; Makropoulos, Antonios; Lötjönen, Jyrki; Menon, David K; Rueckert, Daniel

    2015-04-01

    We propose a framework for the robust and fully-automatic segmentation of magnetic resonance (MR) brain images called "Multi-Atlas Label Propagation with Expectation-Maximisation based refinement" (MALP-EM). The presented approach is based on a robust registration approach (MAPER), highly performant label fusion (joint label fusion) and intensity-based label refinement using EM. We further adapt this framework to be applicable for the segmentation of brain images with gross changes in anatomy. We propose to account for consistent registration errors by relaxing anatomical priors obtained by multi-atlas propagation and a weighting scheme to locally combine anatomical atlas priors and intensity-refined posterior probabilities. The method is evaluated on a benchmark dataset used in a recent MICCAI segmentation challenge. In this context we show that MALP-EM is competitive for the segmentation of MR brain scans of healthy adults when compared to state-of-the-art automatic labelling techniques. To demonstrate the versatility of the proposed approach, we employed MALP-EM to segment 125 MR brain images into 134 regions from subjects who had sustained traumatic brain injury (TBI). We employ a protocol to assess segmentation quality if no manual reference labels are available. Based on this protocol, three independent, blinded raters confirmed on 13 MR brain scans with pathology that MALP-EM is superior to established label fusion techniques. We visually confirm the robustness of our segmentation approach on the full cohort and investigate the potential of derived symmetry-based imaging biomarkers that correlate with and predict clinically relevant variables in TBI such as the Marshall Classification (MC) or Glasgow Outcome Score (GOS). Specifically, we show that we are able to stratify TBI patients with favourable outcomes from non-favourable outcomes with 64.7% accuracy using acute-phase MR images and 66.8% accuracy using follow-up MR images. Furthermore, we are able to

  3. Language and memory profiles of adolescents with traumatic brain injury.

    PubMed

    Moran, Catherine; Gillon, Gail

    2004-03-01

    The performance of adolescents who suffered a traumatic brain injury in childhood, on language comprehension tasks with varying working memory demands, was examined. It was hypothesized that adolescents with a traumatic brain injury would perform more poorly than their non-injured peers, particularly on those tasks with high working memory demands. A case study design allowed for both group and intra-participant comparisons. A battery of language comprehension and working memory tasks was administered to six adolescents aged 12-16 years. Their performance was compared with six individually age-matched peers with typical development and to the normative data of the standardized tests. Intra-participant performance was examined by comparing results across language tasks that varied in working memory demands. Analysis revealed that individuals with traumatic brain injury performed poorly compared with their age-matched peers. However, the pattern of listening comprehension impairment differed across individuals and marked variability within the comprehension profiles for some individuals with traumatic brain injury was evident. Language comprehension tasks with high working memory demands generally posed the most difficulty for individuals with traumatic brain injury. PMID:14726286

  4. Attenuated traumatic axonal injury and improved functional outcome after traumatic brain injury in mice lacking Sarm1.

    PubMed

    Henninger, Nils; Bouley, James; Sikoglu, Elif M; An, Jiyan; Moore, Constance M; King, Jean A; Bowser, Robert; Freeman, Marc R; Brown, Robert H

    2016-04-01

    Axonal degeneration is a critical, early event in many acute and chronic neurological disorders. It has been consistently observed after traumatic brain injury, but whether axon degeneration is a driver of traumatic brain injury remains unclear. Molecular pathways underlying the pathology of traumatic brain injury have not been defined, and there is no efficacious treatment for traumatic brain injury. Here we show that mice lacking the mouse Toll receptor adaptor Sarm1 (sterile α/Armadillo/Toll-Interleukin receptor homology domain protein) gene, a key mediator of Wallerian degeneration, demonstrate multiple improved traumatic brain injury-associated phenotypes after injury in a closed-head mild traumatic brain injury model. Sarm1(-/-) mice developed fewer β-amyloid precursor protein aggregates in axons of the corpus callosum after traumatic brain injury as compared to Sarm1(+/+) mice. Furthermore, mice lacking Sarm1 had reduced plasma concentrations of the phophorylated axonal neurofilament subunit H, indicating that axonal integrity is maintained after traumatic brain injury. Strikingly, whereas wild-type mice exibited a number of behavioural deficits after traumatic brain injury, we observed a strong, early preservation of neurological function in Sarm1(-/-) animals. Finally, using in vivo proton magnetic resonance spectroscopy we found tissue signatures consistent with substantially preserved neuronal energy metabolism in Sarm1(-/-) mice compared to controls immediately following traumatic brain injury. Our results indicate that the SARM1-mediated prodegenerative pathway promotes pathogenesis in traumatic brain injury and suggest that anti-SARM1 therapeutics are a viable approach for preserving neurological function after traumatic brain injury. PMID:26912636

  5. Attenuated traumatic axonal injury and improved functional outcome after traumatic brain injury in mice lacking Sarm1.

    PubMed

    Henninger, Nils; Bouley, James; Sikoglu, Elif M; An, Jiyan; Moore, Constance M; King, Jean A; Bowser, Robert; Freeman, Marc R; Brown, Robert H

    2016-04-01

    Axonal degeneration is a critical, early event in many acute and chronic neurological disorders. It has been consistently observed after traumatic brain injury, but whether axon degeneration is a driver of traumatic brain injury remains unclear. Molecular pathways underlying the pathology of traumatic brain injury have not been defined, and there is no efficacious treatment for traumatic brain injury. Here we show that mice lacking the mouse Toll receptor adaptor Sarm1 (sterile α/Armadillo/Toll-Interleukin receptor homology domain protein) gene, a key mediator of Wallerian degeneration, demonstrate multiple improved traumatic brain injury-associated phenotypes after injury in a closed-head mild traumatic brain injury model. Sarm1(-/-) mice developed fewer β-amyloid precursor protein aggregates in axons of the corpus callosum after traumatic brain injury as compared to Sarm1(+/+) mice. Furthermore, mice lacking Sarm1 had reduced plasma concentrations of the phophorylated axonal neurofilament subunit H, indicating that axonal integrity is maintained after traumatic brain injury. Strikingly, whereas wild-type mice exibited a number of behavioural deficits after traumatic brain injury, we observed a strong, early preservation of neurological function in Sarm1(-/-) animals. Finally, using in vivo proton magnetic resonance spectroscopy we found tissue signatures consistent with substantially preserved neuronal energy metabolism in Sarm1(-/-) mice compared to controls immediately following traumatic brain injury. Our results indicate that the SARM1-mediated prodegenerative pathway promotes pathogenesis in traumatic brain injury and suggest that anti-SARM1 therapeutics are a viable approach for preserving neurological function after traumatic brain injury.

  6. Salutary Effects of Estrogen Sulfate for Traumatic Brain Injury

    PubMed Central

    Kim, Hyunki; Cam-Etoz, Betul; Zhai, Guihua; Hubbard, William J.; Zinn, Kurt R.

    2015-01-01

    Abstract Estrogen plays an important role as a neuroprotector in the central nervous system (CNS), directly interacting with neurons and regulating physiological properties of non-neuronal cells. Here we evaluated estrogen sulfate (E2-SO4) for traumatic brain injury (TBI) using a Sprague–Dawley rat model. TBI was induced via lateral fluid percussion (LFP) at 24 h after craniectomy. E2-SO4 (1 mg/kg BW in 1 mL/kg BW) or saline (served as control) was intravenously administered at 1 h after TBI (n=5/group). Intracranial pressure (ICP), cerebral perfusion pressure (CPP), and partial brain oxygen pressure (pbtO2) were measured for 2 h (from 23 to 25 h after E2-SO4 injection). Brain edema and diffuse axonal injury (DAI) were assessed by diffusion tensor imaging (DTI), and cerebral glycolysis was measured by 18F-labeled fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging, at 1 and 7 days after E2-SO4 injection. E2-SO4 significantly decreased ICP, while increasing CPP and pbtO2 (p<0.05) as compared with vehicle-treated TBI rats. The edema size in the brains of the E2-SO4 treated group was also significantly smaller than that of vehicle-treated group at 1 day after E2-SO4 injection (p=0.04), and cerebral glycolysis of injured region was also increased significantly during the same time period (p=0.04). However, E2-SO4 treatment did not affect DAI (p>0.05). These findings demonstrated the potential benefits of E2-SO4 in TBI. PMID:25646701

  7. Graph analysis of functional brain networks for cognitive control of action in traumatic brain injury.

    PubMed

    Caeyenberghs, Karen; Leemans, Alexander; Heitger, Marcus H; Leunissen, Inge; Dhollander, Thijs; Sunaert, Stefan; Dupont, Patrick; Swinnen, Stephan P

    2012-04-01

    Patients with traumatic brain injury show clear impairments in behavioural flexibility and inhibition that often persist beyond the time of injury, affecting independent living and psychosocial functioning. Functional magnetic resonance imaging studies have shown that patients with traumatic brain injury typically show increased and more broadly dispersed frontal and parietal activity during performance of cognitive control tasks. We constructed binary and weighted functional networks and calculated their topological properties using a graph theoretical approach. Twenty-three adults with traumatic brain injury and 26 age-matched controls were instructed to switch between coordination modes while making spatially and temporally coupled circular motions with joysticks during event-related functional magnetic resonance imaging. Results demonstrated that switching performance was significantly lower in patients with traumatic brain injury compared with control subjects. Furthermore, although brain networks of both groups exhibited economical small-world topology, altered functional connectivity was demonstrated in patients with traumatic brain injury. In particular, compared with controls, patients with traumatic brain injury showed increased connectivity degree and strength, and higher values of local efficiency, suggesting adaptive mechanisms in this group. Finally, the degree of increased connectivity was significantly correlated with poorer switching task performance and more severe brain injury. We conclude that analysing the functional brain network connectivity provides new insights into understanding cognitive control changes following brain injury.

  8. Predicting outcome in traumatic brain injury: Sharing experience of pilot traumatic brain injury registry

    PubMed Central

    Pal, Ranabir; Munivenkatappa, Ashok; Agrawal, Amit; Menon, Geetha R.; Galwankar, Sagar; Mohan, P. Rama; Kumar, S. Satish; Subrahmanyam, B. V.

    2016-01-01

    Background: A reliable prediction of outcome for the victims of traumatic brain injury (TBI) on admission is possible from concurrent data analysis from any systematic real-time registry. Objective: To determine the clinical relevance of the findings from our TBI registry to develop prognostic futuristic models with readily available traditional and novel predictors. Materials and Methods: Prospectively collected data using predesigned pro forma were analyzed from the first phase of a trauma registry from a South Indian Trauma Centre, compatible with computerized management system at electronic data entry and web data entry interface on demographics, clinical, management, and discharge status. Statistical Analysis: On univariate analysis, the variables with P < 0.15 were chosen for binary logistic model. On regression model, variables were selected with test of coefficient 0.001 and with Nagelkerke R2 with alpha error of 5%. Results: From 337 cases, predominantly males from rural areas in their productive age, road traffic injuries accounted for two-thirds cases, one-fourths occurred during postmonsoon while two-wheeler was the most common prerequisite. Fifty percent of patients had moderate to severe brain injury; the most common finding was unconsciousness followed by vomiting, ear bleed, seizures, and traumatic amnesia. Fifteen percent required intracranial surgery. Patients with severe Glasgow coma scale score were 4.5 times likely to have the fatal outcome (P = 0.003). Other important clinical variables accountable for fatal outcomes were oral bleeds and cervical spine injury while imperative socio-demographic risk correlates were age and seasons. Conclusion: TBI registry helped us finding predictors of clinical relevance for the outcomes in victims of TBI in search of prognostic futuristic models in TBI victims. PMID:27722114

  9. Glutamate and GABA imbalance following traumatic brain injury

    PubMed Central

    Guerriero, Réjean M.; Giza, Christopher C.; Rotenberg, Alexander

    2015-01-01

    Traumatic brain injury (TBI) leads to multiple short and long term changes in neuronal circuits that ultimately conclude with an imbalance of cortical excitation and inhibition. Changes in neurotransmitter concentrations, receptor populations and specific cell survival are important contributing factors. Many of these changes occur gradually, which may explain the vulnerability of the brain to multiple mild impacts, alterations in neuroplasticity, and delays in the presentation of post-traumatic epilepsy. In this review we provide an overview of normal glutamate and GABA homeostasis, and describe acute, subacute and chronic changes that follow injury. We conclude by highlighting opportunities for therapeutic interventions in this paradigm. PMID:25796572

  10. Erythropoietin Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy.

    PubMed

    Bramlett, Helen M; Dietrich, W Dalton; Dixon, C Edward; Shear, Deborah A; Schmid, Kara E; Mondello, Stefania; Wang, Kevin K W; Hayes, Ronald L; Povlishock, John T; Tortella, Frank C; Kochanek, Patrick M

    2016-03-15

    Experimental studies targeting traumatic brain injury (TBI) have reported that erythropoietin (EPO) is an endogenous neuroprotectant in multiple models. In addition to its neuroprotective effects, it has also been shown to enhance reparative processes including angiogenesis and neurogenesis. Based on compelling pre-clinical data, EPO was tested by the Operation Brain Trauma Therapy (OBTT) consortium to evaluate therapeutic potential in multiple TBI models along with biomarker assessments. Based on the pre-clinical TBI literature, two doses of EPO (5000 and 10,000 IU/kg) were tested given at 15 min after moderate fluid percussion brain injury (FPI), controlled cortical impact (CCI), or penetrating ballistic-like brain injury (PBBI) with subsequent behavioral, histopathological, and biomarker outcome assessments. There was a significant benefit on beam walk with the 5000 IU dose in CCI, but no benefit on any other motor task across models in OBTT. Also, no benefit of EPO treatment across the three TBI models was noted using the Morris water maze to assess cognitive deficits. Lesion volume analysis showed no treatment effects after either FPI or CCI; however, with the 5000 IU/kg dose of EPO, a paradoxical increase in lesion volume and percent hemispheric tissue loss was seen after PBBI. Biomarker assessments included measurements of glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1) in blood at 4 or 24 h after injury. No treatment effects were seen on biomarker levels after FPI, whereas treatment at either dose exacerbated the increase in GFAP at 24 h in PBBI but attenuated 24-4 h delta UCH-L1 levels at high dose in CCI. Our data indicate a surprising lack of efficacy of EPO across three established TBI models in terms of behavioral, histopathological, and biomarker assessments. Although we cannot rule out the possibility that other doses or more prolonged treatment could show different effects, the lack of efficacy of EPO reduced

  11. Erythropoietin Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy.

    PubMed

    Bramlett, Helen M; Dietrich, W Dalton; Dixon, C Edward; Shear, Deborah A; Schmid, Kara E; Mondello, Stefania; Wang, Kevin K W; Hayes, Ronald L; Povlishock, John T; Tortella, Frank C; Kochanek, Patrick M

    2016-03-15

    Experimental studies targeting traumatic brain injury (TBI) have reported that erythropoietin (EPO) is an endogenous neuroprotectant in multiple models. In addition to its neuroprotective effects, it has also been shown to enhance reparative processes including angiogenesis and neurogenesis. Based on compelling pre-clinical data, EPO was tested by the Operation Brain Trauma Therapy (OBTT) consortium to evaluate therapeutic potential in multiple TBI models along with biomarker assessments. Based on the pre-clinical TBI literature, two doses of EPO (5000 and 10,000 IU/kg) were tested given at 15 min after moderate fluid percussion brain injury (FPI), controlled cortical impact (CCI), or penetrating ballistic-like brain injury (PBBI) with subsequent behavioral, histopathological, and biomarker outcome assessments. There was a significant benefit on beam walk with the 5000 IU dose in CCI, but no benefit on any other motor task across models in OBTT. Also, no benefit of EPO treatment across the three TBI models was noted using the Morris water maze to assess cognitive deficits. Lesion volume analysis showed no treatment effects after either FPI or CCI; however, with the 5000 IU/kg dose of EPO, a paradoxical increase in lesion volume and percent hemispheric tissue loss was seen after PBBI. Biomarker assessments included measurements of glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1) in blood at 4 or 24 h after injury. No treatment effects were seen on biomarker levels after FPI, whereas treatment at either dose exacerbated the increase in GFAP at 24 h in PBBI but attenuated 24-4 h delta UCH-L1 levels at high dose in CCI. Our data indicate a surprising lack of efficacy of EPO across three established TBI models in terms of behavioral, histopathological, and biomarker assessments. Although we cannot rule out the possibility that other doses or more prolonged treatment could show different effects, the lack of efficacy of EPO reduced

  12. Glibenclamide reduces secondary brain damage after experimental traumatic brain injury.

    PubMed

    Zweckberger, K; Hackenberg, K; Jung, C S; Hertle, D N; Kiening, K L; Unterberg, A W; Sakowitz, O W

    2014-07-11

    Following traumatic brain injury (TBI) SUR1-regulated NCCa-ATP (SUR1/TRPM4) channels are transcriptionally up-regulated in ischemic astrocytes, neurons, and capillaries. ATP depletion results in depolarization and opening of the channel leading to cytotoxic edema. Glibenclamide is an inhibitor of SUR-1 and, thus, might prevent cytotoxic edema and secondary brain damage following TBI. Anesthetized adult Sprague-Dawley rats underwent parietal craniotomy and were subjected to controlled cortical impact injury (CCI). Glibenclamide was administered as a bolus injection 15min after CCI injury and continuously via osmotic pumps throughout 7days. In an acute trial (180min) mean arterial blood pressure, heart rate, intracranial pressure, encephalographic activity, and cerebral metabolism were monitored. Brain water content was assessed gravimetrically 24h after CCI injury and contusion volumes were measured by MRI scanning technique at 8h, 24h, 72h, and 7d post injury. Throughout the entire time of observation neurological function was quantified using the "beam-walking" test. Glibenclamide-treated animals showed a significant reduction in the development of brain tissue water content(80.47%±0.37% (glibenclamide) vs. 80.83%±0.44% (control); p<0.05; n=14). Contusion sizes increased continuously within 72h following CCI injury, but glibenclamide-treated animals had significantly smaller volumes at any time-points, like 172.53±38.74mm(3) (glibenclamide) vs. 299.20±64.02mm(3) (control) (p<0.01; n=10; 24h) or 211.10±41.03mm(3) (glibenclamide) vs. 309.76±19.45mm(3) (control) (p<0.05; n=10; 72h), respectively. An effect on acute parameters, however, could not be detected, most likely because of the up-regulation of the channel within 3-6h after injury. Furthermore, there was no significant effect on motor function assessed by the beam-walking test throughout 7days. In accordance to these results and the available literature, glibenclamide seems to have promising potency in

  13. Serum sodium disorders in patients with traumatic brain injury

    PubMed Central

    Paiva, Wellingson Silva; Bezerra, Douglas Alexandre França; Amorim, Robson Luis Oliveira; Figueiredo, Eberval Gadelha; Tavares, Wagner Malago; De Andrade, Almir Ferreira; Teixeira, Manoel Jacobsen

    2011-01-01

    Sodium disorders are the most common and most poorly understood electrolyte disorders in neurological patients. The aim of this study was to determine the incidence of sodium disorders and its association with different traumatic brain injuries. This prospective study was conducted in 80 patients diagnosed with moderate and severe traumatic brain injuries. All patients underwent cerebral computed tomography. Incidence of sodium disorders, presence of injuries in the first computed tomography after traumatic brain injury, and level of consciousness were analyzed. Patients that presented other potential causes of sodium disorders and systemic trauma were excluded from the study. The incidence of sodium disturbances was 45%: 20 patients presented hypernatremia and 16 hyponatremia. Refers to all patients with sodium disturbances 53% were detected in the first sample. We recorded at least one measurement <125 mEq/L in 50% of the patients with hyponatremia. A greater incidence of sodium disorders was found in patients with subdural, intracerebral hematoma and with diffuse axonal injury. The incidence of sodium disorders among the patients with diffuse lesions was greater than in the group of patients with brain contusion (P = 0.022). The incidence of sodium disorders is higher in patients with diffuse traumatic brain injuries. No association was found between focal lesions and proportion of sodium disorders. PMID:21941440

  14. 78 FR 76196 - Secondary Service Connection for Diagnosable Illnesses Associated With Traumatic Brain Injury

    Federal Register 2010, 2011, 2012, 2013, 2014

    2013-12-17

    ... Traumatic Brain Injury AGENCY: Department of Veterans Affairs. ACTION: Final rule. SUMMARY: The Department... and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury, regarding the association between traumatic brain injury (TBI) and five diagnosable illnesses. This amendment establishes that if...

  15. 78 FR 9929 - Current Traumatic Brain Injury State Implementation Partnership Grantees; Non-Competitive One...

    Federal Register 2010, 2011, 2012, 2013, 2014

    2013-02-12

    ... HUMAN SERVICES Health Resources and Services Administration Current Traumatic Brain Injury State...-Competitive One-Year Extension Funds for Current Traumatic Brain Injury (TBI) State Implementation Partnership... by the Traumatic Brain Injury Act of 1996 (Pub. L. 104-166) and was most recently reauthorized by...

  16. Neuroprotective effects of vagus nerve stimulation on traumatic brain injury

    PubMed Central

    Zhou, Long; Lin, Jinhuang; Lin, Junming; Kui, Guoju; Zhang, Jianhua; Yu, Yigang

    2014-01-01

    Previous studies have shown that vagus nerve stimulation can improve the prognosis of traumatic brain injury. The aim of this study was to elucidate the mechanism of the neuroprotective effects of vagus nerve stimulation in rabbits with brain explosive injury. Rabbits with brain explosive injury received continuous stimulation (10 V, 5 Hz, 5 ms, 20 minutes) of the right cervical vagus nerve. Tumor necrosis factor-α, interleukin-1β and interleukin-10 concentrations were detected in serum and brain tissues, and water content in brain tissues was measured. Results showed that vagus nerve stimulation could reduce the degree of brain edema, decrease tumor necrosis factor-α and interleukin-1β concentrations, and increase interleukin-10 concentration after brain explosive injury in rabbits. These data suggest that vagus nerve stimulation may exert neuroprotective effects against explosive injury via regulating the expression of tumor necrosis factor-α, interleukin-1β and interleukin-10 in the serum and brain tissue. PMID:25368644

  17. Traumatic brain injury: neuroprotective anaesthetic techniques, an update.

    PubMed

    Tawfeeq, Nasser A; Halawani, Mohammed M; Al-Faridi, Khulood; Aal-Shaya, Wa'el A; Taha, Wa'el S

    2009-11-01

    Traumatic brain injuries remain an area of great challenge to both neurosurgeons and neuroanaesthesiologists. The management of these injuries starts at the scene of the accident. However, strategies for preventing secondary brain injury and its sequelae are continuing to evolve. These strategies include the use of pharmacological and nonpharmacological techniques. Preventing hypoxia and the use of hypertonic saline have been shown to have favourable results on the outcome of these injuries. The use of isoflurane has been shown to have a neuronprotective effect. Propofol is thought to be the future drug of choice because of its neuroprotective properties, although these still need to be further proven through research. In this review an understanding of the pathophysiology of traumatic brain injury will be outlined in order to understand the effects of pharmacological and nonpharmacological agents on secondary brain injury. PMID:19895957

  18. The History and Evolution of Experimental Traumatic Brain Injury Models.

    PubMed

    Povlishock, John

    2016-01-01

    This narrative provides a brief history of experimental animal model development for the study of traumatic brain injury. It draws upon a relatively rich history of early animal modeling that employed higher order animals to assess concussive brain injury while exploring the importance of head movement versus stabilization in evaluating the animal's response to injury. These themes are extended to the development of angular/rotational acceleration/deceleration models that also exploited brain movement to generate both the morbidity and pathology typically associated with human traumatic brain injury. Despite the significance of these early model systems, their limitations and overall practicality are discussed. Consideration is given to more contemporary rodent animal models that replicate individual/specific features of human injury, while via various transgenic technologies permitting the evaluation of injury-mediated pathways. The narrative closes on a reconsideration of higher order, porcine animal models of injury and their implication for preclinical/translational research. PMID:27604709

  19. Traumatic Brain Injury Detection Using Electrophysiological Methods

    PubMed Central

    Rapp, Paul E.; Keyser, David O.; Albano, Alfonso; Hernandez, Rene; Gibson, Douglas B.; Zambon, Robert A.; Hairston, W. David; Hughes, John D.; Krystal, Andrew; Nichols, Andrew S.

    2015-01-01

    Measuring neuronal activity with electrophysiological methods may be useful in detecting neurological dysfunctions, such as mild traumatic brain injury (mTBI). This approach may be particularly valuable for rapid detection in at-risk populations including military service members and athletes. Electrophysiological methods, such as quantitative electroencephalography (qEEG) and recording event-related potentials (ERPs) may be promising; however, the field is nascent and significant controversy exists on the efficacy and accuracy of the approaches as diagnostic tools. For example, the specific measures derived from an electroencephalogram (EEG) that are most suitable as markers of dysfunction have not been clearly established. A study was conducted to summarize and evaluate the statistical rigor of evidence on the overall utility of qEEG as an mTBI detection tool. The analysis evaluated qEEG measures/parameters that may be most suitable as fieldable diagnostic tools, identified other types of EEG measures and analysis methods of promise, recommended specific measures and analysis methods for further development as mTBI detection tools, identified research gaps in the field, and recommended future research and development thrust areas. The qEEG study group formed the following conclusions: (1) Individual qEEG measures provide limited diagnostic utility for mTBI. However, many measures can be important features of qEEG discriminant functions, which do show significant promise as mTBI detection tools. (2) ERPs offer utility in mTBI detection. In fact, evidence indicates that ERPs can identify abnormalities in cases where EEGs alone are non-disclosing. (3) The standard mathematical procedures used in the characterization of mTBI EEGs should be expanded to incorporate newer methods of analysis including non-linear dynamical analysis, complexity measures, analysis of causal interactions, graph theory, and information dynamics. (4) Reports of high specificity in q

  20. Seizures and the Role of Anticonvulsants After Traumatic Brain Injury.

    PubMed

    Zimmermann, Lara L; Diaz-Arrastia, Ramon; Vespa, Paul M

    2016-10-01

    Posttraumatic seizures are a common complication of traumatic brain injury. Posttraumatic epilepsy accounts for 20% of symptomatic epilepsy in the general population and 5% of all epilepsy. Early posttraumatic seizures occur in more than 20% of patients in the intensive care unit and are associated with secondary brain injury and worse patient outcomes. Most posttraumatic seizures are nonconvulsive and therefore continuous electroencephalography monitoring should be the standard of care for patients with moderate or severe brain injury. The literature shows that posttraumatic seizures result in secondary brain injury caused by increased intracranial pressure, cerebral edema and metabolic crisis. PMID:27637399

  1. Mild traumatic brain injury does not produce post-traumatic stress disorder.

    PubMed

    Sbordone, R J; Liter, J C

    1995-01-01

    It has been widely assumed that patients who sustain mild traumatic brain injury (MTBI) or post-concussive syndrome develop post-traumatic stress disorder (PTSD) in response to their cognitive difficulties, diminished coping skills, or other losses. This study examined 70 patients who had previously been diagnosed as having either PTSD or MTBI. Each patient was asked to provide a highly detailed chronological history of the events which preceded, followed, and occurred during the traumatic event, to indicate whether they were rendered unconscious or had amnesia for the event, and to describe the various symptoms they developed. All (100.0%) of the PTSD patients were able to provide a highly detailed and emotionally charged recollection of the events which occurred within 15 minutes of the traumatic event in comparison to none (0.0%) of the MTBI patients. None of the MTBI patients reported symptoms such as intrusive recollections of the traumatic event, nightmares, hypervigilance, phobic or startle reactions, or became upset when they were asked to describe the traumatic event or were exposed to stimuli associated with it. These data suggest that PTSD and MTBI are two mutually exclusive disorders, and that it is highly unlikely that MTBI patients develop PTSD symptoms. Furthermore, these findings suggest that clinicians should exercise considerable caution in ruling out PTSD prior to making the diagnosis of MTBI. PMID:7640686

  2. Cytokine Gene Polymorphisms and Outcome after Traumatic Brain Injury

    PubMed Central

    Waters, Ryan J.; Murray, Gordon D.; Teasdale, Graham M.; Stewart, Janice; Day, Ian; Lee, Robert J.

    2013-01-01

    Abstract Clinical outcome after traumatic brain injury (TBI) is variable and cannot easily be predicted. There is increasing evidence to suggest that there may be genetic influences on outcome. Cytokines play an important role in mediating the inflammatory response provoked within the central nervous system after TBI. This study was designed to identify associations between cytokine gene polymorphisms and clinical outcome 6 months after head injury. A prospectively identified cohort of patients (n=1096, age range 0–93 years, mean age 37) was used. Clinical outcome at 6 months was assessed using the Glasgow Outcome Scale. In an initial screen of 11 cytokine gene single nucleotide polymorphisms (SNPs) previously associated with disease susceptibility or outcome (TNFA −238 and −308, IL6 −174, −572 and −597, IL1A −889, IL1B −31, −511 and +3953, and TGFB −509 and −800), TNFA −308 was identified as having a likely association. The TNFA −308 SNP was further evaluated, and a significant association was identified, with 39% of allele 2 carriers having an unfavorable outcome compared with 31% of non-carriers (adjusted odds ratio 1.67, confidence interval 1.19–2.35, p=0.003). These findings are consistent with experimental and clinical data suggesting that neuroinflammation has an impact on clinical outcome after TBI and that tumor necrosis factor alpha plays an important role in this process. PMID:23768161

  3. Chaperone-Mediated Autophagy after Traumatic Brain Injury

    PubMed Central

    Park, Yujung; Liu, Chunli; Luo, Tianfei; Dietrich, W. Dalton; Bramlett, Helen

    2015-01-01

    Abstract Chaperone-mediated autophagy (CMA) and the ubiquitin-proteasomal system (UPS) are two major protein degradation systems responsible for maintaining cellular homeostasis, but how these two systems are regulated after traumatic brain injury (TBI) remains unknown. TBI produces primary mechanical damage that must be repaired to maintain neuronal homeostasis. The level of lysosomal-associated membrane protein type 2A (LAMP2A) is the hallmark of CMA activity. The level of polyubiquitinated proteins (ubi-proteins) reflects UPS activity. This study utilized a moderate fluid percussion injury model in rats to investigate the changes in CMA and the UPS after TBI. Induction of CMA was manifested by significant upregulation of LAMP2A and secondary lysosomes during the periods of 1–15 days of recovery after TBI. In comparison, the levels of ubi-proteins were increased only moderately after TBI. The increases in the levels of LAMP2A and 70 kDa heat-shock protein for CMA after TBI were seen mainly in the secondary lysosome-containing fractions. Confocal and electron microscopy further showed that increased LAMP2A or lysosomes were found mainly in neurons and proliferated microglia. Because CMA and the UPS are two major routes for elimination of different types of cellular aberrant proteins, the consecutive activation of these two pathways may serve as a protective mechanism for maintaining cellular homeostasis after TBI. PMID:25891649

  4. Toward an International Initiative for Traumatic Brain Injury Research

    PubMed Central

    Tosetti, Patrizia; Theriault, Elizabeth; Phillips, Anthony; Koroshetz, Walter; Draghia-Akli, Ruxandra

    2013-01-01

    Abstract The European Commission (EC) and the National Institutes of Health (NIH) jointly sponsored a workshop on October 18–20, 2011 in Brussels to discuss the feasibility and benefits of an international collaboration in the field of traumatic brain injury (TBI) research. The workshop brought together scientists, clinicians, patients, and industry representatives from around the globe as well as funding agencies from the EU, Spain, the United States, and Canada. Sessions tackled both the possible goals and governance of a future initiative and the scientific questions that would most benefit from an integrated international effort: how to optimize data collection and sharing; injury classification; outcome measures; clinical study design; and statistical analysis. There was a clear consensus that increased dialogue and coordination of research at an international level would be beneficial for advancing TBI research, treatment, and care. To this end, the EC, the NIH, and the Canadian Institutes of Health Research expressed interest in developing a framework for an international initiative for TBI Research (InTBIR). The workshop participants recommended that InTBIR initially focus on collecting, standardizing, and sharing clinical TBI data for comparative effectiveness research, which will ultimately result in better management and treatments for TBI. PMID:23731282

  5. Evaluation of a Health Education Programme about Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Garcia, Jane Mertz; Sellers, Debra M.; Hilgendorf, Amy E.; Burnett, Debra L.

    2014-01-01

    Objective: Our aim was to evaluate a health education programme (TBIoptions: Promoting Knowledge) designed to increase public awareness and understanding about traumatic brain injury (TBI) through in-person (classroom) and computer-based (electronic) learning environments. Design: We used a pre-post survey design with randomization of participants…

  6. Decompressive Craniectomy and Traumatic Brain Injury: A Review

    PubMed Central

    Alvis-Miranda, Hernando; Castellar-Leones, Sandra Milena; Moscote-Salazar, Luis Rafael

    2013-01-01

    Intracranial hypertension is the largest cause of death in young patients with severe traumatic brain injury. Decompressive craniectomy is part of the second level measures for the management of increased intracranial pressure refractory to medical management as moderate hypothermia and barbiturate coma. The literature lack of concepts is their indications. We present a review on the state of the art. PMID:27162826

  7. Memory Strategies to Use With Students Following Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Pershelli, Andi

    2007-01-01

    Following a traumatic brain injury, including a mild concussion, most students will have some degree of memory impairment. It can take 1-3 years for a child's memory to improve to its maximum capability following injury. Children cannot wait that long before returning to school. Teachers need to know how to diversify their instruction in order to…

  8. Traumatic Brain Injury and Its Effect on Students

    ERIC Educational Resources Information Center

    Rosenthal, Stacy B.

    2012-01-01

    Over one million people suffer a traumatic brain injury every year, many of whom are students between the ages of 5 and 18. Using a qualitative case study approach, I wanted to discover the specific factors that both impede and help the school re-entry process for students in grades kindergarten through twelve so that these students can return to…

  9. Performance Monitoring in Children following Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Ornstein, Tisha J.; Levin, Harvey S.; Chen, Shirley; Hanten, Gerri; Ewing-Cobbs, Linda; Dennis, Maureen; Barnes, Marcia; Max, Jeffrey E.; Logan, Gordon D.; Schachar, Russell

    2009-01-01

    Background: Executive control deficits are common sequelae of childhood traumatic brain injury (TBI). The goal of the current study was to assess a specific executive control function, performance monitoring, in children following TBI. Methods: Thirty-one children with mild-moderate TBI, 18 with severe TBI, and 37 control children without TBI, of…

  10. Pediatric Traumatic Brain Injury. Special Topic Report #3.

    ERIC Educational Resources Information Center

    Waaland, Pamela K.; Cockrell, Janice L.

    This brief report summarizes what is known about pediatric traumatic brain injury, including the following: risk factors (e.g., males especially those ages 5 to 25, youth with preexisting problems including previous head injury victims, and children receiving inadequate supervision); life after injury; physical and neurological consequences (e.g.,…

  11. Legal Challenges in Educating Traumatic Brain Injured Students.

    ERIC Educational Resources Information Center

    Martin, Reed

    1988-01-01

    Since most children with traumatic brain injury (TBI) were not previously in special education, their entitlement to special services, their parents' role in securing those services, and the school district's perception of them as disabled will be new. Both parents and regular school personnel may be resistant to special educational services. (DB)

  12. Management of Attention and Memory Disorders Following Traumatic Brain Injury.

    ERIC Educational Resources Information Center

    Mateer, Catherine A.; And Others

    1996-01-01

    Disorders of attention, memory, and executive function are common sequelae of traumatic brain injuries in children. Intervention usually involves externally focused interventions aimed at changing the environment to minimize the dysfunction; internally focused interventions aimed at improving the underlying cognitive ability; or compensatory…

  13. Predictors of Neuropsychological Test Performance After Pediatric Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Donders, Jacobus; Nesbit-Greene, Kelly

    2004-01-01

    The influence of neurological and demographic variables on neuropsychological test performance was examined in 100 9- to 16-year-old children with traumatic brain injury (TBI). Regression analyses were conducted to determine the relative contributions of coma, neuroimaging findings, ethnicity, socioeconomic status, and gender to variance in…

  14. Narrative Skills Following Traumatic Brain Injury in Children and Adults.

    ERIC Educational Resources Information Center

    Biddle, Kathleen R.; And Others

    1996-01-01

    This study used dependency analysis to document and describe the narrative discourse impairments of 10 children (mean age 12) and 10 adults (mean age 35) with traumatic brain injury (TBI), and matched controls. Individuals with TBI were significantly more disfluent than controls and their narrative performance required a significant listener…

  15. Collaborative Intervention in Schools after Traumatic Brain Injury.

    ERIC Educational Resources Information Center

    Szekeres, Shirley F.; Meserve, Nancy F.

    1994-01-01

    This article discusses principles and procedures of collaborative intervention in delivering educational services for children with traumatic brain injury (TBI). The article presents examples of metacognitive-communicative intervention that can be carried out through collaboration across the school day and describes episodes of collaborative…

  16. Classroom Interventions for Students with Traumatic Brain Injuries

    ERIC Educational Resources Information Center

    Bowen, Julie M.

    2005-01-01

    Students who have sustained a traumatic brain injury (TBI) return to the school setting with a range of cognitive, psychosocial, and physical deficits that can significantly affect their academic functioning. Successful educational reintegration for students with TBI requires careful assessment of each child's unique needs and abilities and the…

  17. Intervention Strategies for Serving Students with Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Arroyos-Jurado, Elsa; Savage, Todd A.

    2008-01-01

    As school-age children are at the highest risk for sustaining a traumatic brain injury (TBI), educational professionals working in school settings will encounter students dealing with the after-effects of a TBI. These effects can influence students' ability to navigate the behavioral, social, and academic demands of the classroom. This article…

  18. Traumatic Brain Injury: When Children Return to School.

    ERIC Educational Resources Information Center

    Williams, Dennis

    This guide addresses issues concerned with the reintegration of students with traumatic brain injuries (TBI) into the classroom. It first provides a definition of TBI and identifies characteristics of students with TBI. The guide then discusses cognitive consequences of TBI, with emphasis on deficits of executive function, attention, and memory.…

  19. Development of an Ontology for Rehabilitation: Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Grove, Michael J.

    2013-01-01

    Traumatic Brain Injury (TBI) rehabilitation interventions are very heterogeneous due to injury characteristics and pathology, patient demographics, healthcare settings, caregiver variability, and individualized, multi-discipline treatment plans. Consequently, comparing and generalizing the effectiveness of interventions is limited largely due to…

  20. Traumatic Brain Injury: Persistent Misconceptions and Knowledge Gaps among Educators

    ERIC Educational Resources Information Center

    Ettel, Deborah; Glang, Ann E.; Todis, Bonnie; Davies, Susan C.

    2016-01-01

    Each year approximately 700,000 U.S. children aged 0-19 years sustain a traumatic brain injury (TBI) placing them at risk for academic, cognitive, and behavioural challenges. Although TBI has been a special education disability category for 25 years, prevalence studies show that of the 145,000 students each year who sustain long-term injury from…

  1. Assisting Students with a Traumatic Brain Injury in School Interventions

    ERIC Educational Resources Information Center

    Aldrich, Erin M.; Obrzut, John E.

    2012-01-01

    Traumatic brain injury (TBI) in children and adolescents can significantly affect their lives and educational needs. Deficits are often exhibited in areas such as attention, concentration, memory, executive function, emotional regulation, and behavioral functioning, but specific outcomes are not particular to any one child or adolescent with a…

  2. School-Based Traumatic Brain Injury and Concussion Management Program

    ERIC Educational Resources Information Center

    Davies, Susan C.

    2016-01-01

    Traumatic brain injuries (TBIs), including concussions, can result in a constellation of physical, cognitive, emotional, and behavioral symptoms that affect students' well-being and performance at school. Despite these effects, school personnel remain underprepared identify, educate, and assist this population of students. This article describes a…

  3. Traumatic Brain Injury in Early Childhood: Developmental Effects and Interventions.

    ERIC Educational Resources Information Center

    Lowenthal, Barbara; Lowenthal, Barbara

    1998-01-01

    Describes the unique effects of traumatic brain injury (TBI) on development in early childhood and offers suggestions for interventions in the cognitive, language, social-emotional, motor, and adaptive domains. Urges more intensive, long-term studies on the immediate and long-term effects of TBI. (Author/DB)

  4. Early Childhood Traumatic Brain Injuries: Effects on Development and Interventions.

    ERIC Educational Resources Information Center

    Lowenthal, Barbara

    1998-01-01

    Describes the variety of possible effects of traumatic brain injuries (TBI) on early childhood development in the cognitive, language, social-emotional, motor, and adaptive domains. Suggests interventions which can assist young survivors and their families. Suggests that more long-term, intensive studies be conducted on the short- and long-term…

  5. Enhancing the Schooling of Students with Traumatic Brain Injury.

    ERIC Educational Resources Information Center

    Keyser-Marcus, Lori; Briel, Lori; Sherron-Targett, Pam; Yasuda, Satoko; Johnson, Susan; Wehman, Paul

    2002-01-01

    This article explores how to identify students with traumatic brain injury (TBI), difficulties students with TBI may face in the classroom, where the best placements might be, and what teaching strategies are effective. A classroom observation checklist for students with TBI is provided, along with advice on developing instructional plans.…

  6. Predicting Institutionalization after Traumatic Brain Injury Inpatient Rehabilitation

    PubMed Central

    Seel, Ronald T.; Goldstein, Richard; Brown, Allen W.; Watanabe, Thomas K.; Zasler, Nathan D.; Roth, Elliot J.; Zafonte, Ross D.; Glenn, Mel B.

    2015-01-01

    Abstract Risk factors contributing to institutionalization after inpatient rehabilitation for people with traumatic brain injury (TBI) have not been well studied and need to be better understood to guide clinicians during rehabilitation. We aimed to develop a prognostic model that could be used at admission to inpatient rehabilitation facilities to predict discharge disposition. The model could be used to provide the interdisciplinary team with information regarding aspects of patients' functioning and/or their living situation that need particular attention during inpatient rehabilitation if institutionalization is to be avoided. The study population included 7219 patients with moderate-severe TBI in the Traumatic Brain Injury Model Systems (TBIMS) National Database enrolled from 2002–2012 who had not been institutionalized prior to injury. Based on institutionalization predictors in other populations, we hypothesized that among people who had lived at a private residence prior to injury, greater dependence in locomotion, bed-chair-wheelchair transfers, bladder and bowel continence, feeding, and comprehension at admission to inpatient rehabilitation programs would predict institutionalization at discharge. Logistic regression was used, with adjustment for demographic factors, proxy measures for TBI severity, and acute-care length-of-stay. C-statistic and predictiveness curves validated a five-variable model. Higher levels of independence in bladder management (adjusted odds ratio [OR], 0.88; 95% CI 0.83, 0.93), bed-chair-wheelchair transfers (OR, 0.81 [95% CI, 0.83–0.93]), and comprehension (OR, 0.78 [95% CI, 0.68, 0.89]) at admission were associated with lower risks of institutionalization on discharge. For every 10-year increment in age was associated with a 1.38 times higher risk for institutionalization (95% CI, 1.29, 1.48) and living alone was associated with a 2.34 times higher risk (95% CI, 1.86, 2.94). The c-statistic was 0.780. We conclude that this

  7. Analysis of Functional Pathways Altered after Mild Traumatic Brain Injury

    PubMed Central

    Redell, John B.; Moore, Anthony N.; Grill, Raymond J.; Johnson, Daniel; Zhao, Jing; Liu, Yin

    2013-01-01

    Abstract Concussive injury (or mild traumatic brain injury; mTBI) can exhibit features of focal or diffuse injury patterns. We compared and contrasted the cellular and molecular responses after mild controlled cortical impact (mCCI; a focal injury) or fluid percussion injury (FPI; a diffuse injury) in rats. The rationale for this comparative analysis was to investigate the brain's response to mild diffuse versus mild focal injury to identify common molecular changes triggered by these injury modalities and to determine the functional pathways altered after injury that may provide novel targets for therapeutic intervention. Microarrays containing probes against 21,792 unique messenger RNAs (mRNAs) were used to investigate the changes in cortical mRNA expression levels at 3 and 24 h postinjury. Of the 354 mRNAs with significantly altered expression levels after mCCI, over 89% (316 mRNAs) were also contained within the mild FPI (mFPI) data set. However, mFPI initiated a more widespread molecular response, with over 2300 mRNAs differentially expressed. Bioinformatic analysis of annotated Gene Ontology molecular function and biological pathway terms showed a significant overrepresentation of genes belonging to inflammation, stress, and signaling categories in both data sets. We therefore examined changes in the protein levels of a panel of 23 cytokines and chemokines in cortical extracts using a Luminex-based bead immunoassay and detected significant increases in macrophage inflammatory protein (MIP)-1α (CCL3), GRO-KC (CXCL1), interleukin (IL)-1α, IL-1β, and IL-6. Immunohistochemical localization of MIP-1α and IL-1β showed marked increases at 3 h postinjury in the cortical vasculature and microglia, respectively, that were largely resolved by 24 h postinjury. Our findings demonstrate that both focal and diffuse mTBI trigger many shared pathobiological processes (e.g., inflammatory responses) that could be targeted for mechanism-based therapeutic interventions

  8. GFAP-BDP as an Acute Diagnostic Marker in Traumatic Brain Injury: Results from the Prospective Transforming Research and Clinical Knowledge in Traumatic Brain Injury Study

    PubMed Central

    Yue, John K.; Puccio, Ava M.; Panczykowski, David M.; Inoue, Tomoo; McMahon, Paul J.; Sorani, Marco D.; Yuh, Esther L.; Lingsma, Hester F.; Maas, Andrew I.R.; Valadka, Alex B.; Manley, Geoffrey T.; Casey, Scott S.; Cheong, Maxwell; Cooper, Shelly R.; Dams-O'Connor, Kristen; Gordon, Wayne A.; Hricik, Allison J.; Hochberger, Kerri; Menon, David K.; Mukherjee, Pratik; Sinha, Tuhin K.; Schnyer, David M.; Vassar, Mary J.

    2013-01-01

    Abstract Reliable diagnosis of traumatic brain injury (TBI) is a major public health need. Glial fibrillary acidic protein (GFAP) is expressed in the central nervous system, and breakdown products (GFAP-BDP) are released following parenchymal brain injury. Here, we evaluate the diagnostic accuracy of elevated levels of plasma GFAP-BDP in TBI. Participants were identified as part of the prospective Transforming Research And Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI) Study. Acute plasma samples (<24 h post-injury) were collected from patients presenting with brain injury who had CT imaging. The ability of GFAP-BDP level to discriminate patients with demonstrable traumatic lesions on CT, and with failure to return to pre-injury baseline at 6 months, was evaluated by the area under the receiver operating characteristic curve (AUC). Of the 215 patients included for analysis, 83% had mild, 4% had moderate, and 13% had severe TBI; 54% had acute traumatic lesions on CT. The ability of GFAP-BDP level to discriminate patients with traumatic lesions on CT as evaluated by AUC was 0.88 (95% confidence interval [CI], 0.84–0.93). The optimal cutoff of 0.68 ng/mL for plasma GFAP-BDP level was associated with a 21.61 odds ratio for traumatic findings on head CT. Discriminatory ability of unfavorable 6 month outcome was lower, AUC 0.65 (95% CI, 0.55–0.74), with a 2.07 odds ratio. GFAP-BDP levels reliably distinguish the presence and severity of CT scan findings in TBI patients. Although these findings confirm and extend prior studies, a larger prospective trial is still needed to validate the use of GFAP-BDP as a routine diagnostic biomarker for patient care and clinical research. The term “mild” continues to be a misnomer for this patient population, and underscores the need for evolving classification strategies for TBI targeted therapy. (ClinicalTrials.gov number NCT01565551; NIH Grant 1RC2 NS069409) PMID:23489259

  9. Pituitary dysfunction following traumatic brain injury: clinical perspectives

    PubMed Central

    Tanriverdi, Fatih; Kelestimur, Fahrettin

    2015-01-01

    Traumatic brain injury (TBI) is a well recognized public health problem worldwide. TBI has previously been considered as a rare cause of hypopituitarism, but an increased prevalence of neuroendocrine dysfunction in patients with TBI has been reported during the last 15 years in most of the retrospective and prospective studies. Based on data in the current literature, approximately 15%–20% of TBI patients develop chronic hypopituitarism, which clearly suggests that TBI-induced hypopituitarism is frequent in contrast with previous assumptions. This review summarizes the current data on TBI-induced hypopituitarism and briefly discusses some clinical perspectives on post-traumatic anterior pituitary hormone deficiency. PMID:26251600

  10. What does the brain tell us about abstract art?

    PubMed Central

    Aviv, Vered

    2014-01-01

    In this essay I focus on the question of why we are attracted to abstract art (perhaps more accurately, non-representational or object-free art). After elaborating on the processing of visual art in general and abstract art in particular, I discuss recent data from neuroscience and behavioral studies related to abstract art. I conclude with several speculations concerning our apparent appeal to this particular type of art. In particular, I claim that abstract art frees our brain from the dominance of reality, enabling it to flow within its inner states, create new emotional and cognitive associations, and activate brain-states that are otherwise harder to access. This process is apparently rewarding as it enables the exploration of yet undiscovered inner territories of the viewer’s brain. PMID:24616683

  11. Epileptogenesis after traumatic brain injury in Plau-deficient mice.

    PubMed

    Bolkvadze, Tamuna; Rantala, Jukka; Puhakka, Noora; Andrade, Pedro; Pitkänen, Asla

    2015-10-01

    Several components of the urokinase-type plasminogen activator receptor (uPAR)-interactome, including uPAR and its ligand sushi-repeat protein 2, X-linked (SRPX2), are linked to susceptibility to epileptogenesis in animal models and/or humans. Recent evidence indicates that urokinase-type plasminogen activator (uPA), a uPAR ligand with focal proteinase activity in the extracellular matrix, contributes to recovery-enhancing brain plasticity after various epileptogenic insults such as traumatic brain injury (TBI) and status epilepticus. Here, we examined whether deficiency of the uPA-encoding gene Plau augments epileptogenesis after TBI. Traumatic brain injury was induced by controlled cortical impact in the somatosensory cortex of adult male wild-type and Plau-deficient mice. Development of epilepsy and seizure susceptibility were assessed with a 3-week continuous video-electroencephalography monitoring and a pentylenetetrazol test, respectively. Traumatic brain injury-induced cortical or hippocampal pathology did not differ between genotypes. The pentylenetetrazol test revealed increased seizure susceptibility after TBI (p<0.05) in injured mice. Epileptogenesis was not exacerbated, however, in Plau-deficient mice. Taken together, Plau deficiency did not worsen controlled cortical impact-induced brain pathology or epileptogenesis caused by TBI when assessed at chronic timepoints. These data expand previous observations on Plau deficiency in models of status epilepticus and suggest that inhibition of focal extracellular proteinase activity resulting from uPA-uPAR interactions does not modify epileptogenesis after TBI. PMID:26253597

  12. Detecting Behavioral Deficits Post Traumatic Brain Injury in Rats.

    PubMed

    Awwad, Hibah O

    2016-01-01

    Traumatic brain injury (TBI), ranging from mild to severe, almost always elicits an array of behavioral deficits in injured subjects. Some of these TBI-induced behavioral deficits include cognitive and vestibulomotor deficits as well as anxiety and other consequences. Rodent models of TBI have been (and still are) fundamental in establishing many of the pathophysiological mechanisms of TBI. Animal models are also utilized in screening and testing pharmacological effects of potential therapeutic agents for brain injury treatment. This chapter details validated protocols for each of these behavioral deficits post traumatic brain injury in Sprague-Dawley male rats. The elevated plus maze (EPM) protocol is described for assessing anxiety-like behavior; the Morris water maze protocol for assessing cognitive deficits in learning memory and spatial working memory and the rotarod test for assessing vestibulomotor deficits. PMID:27604739

  13. Pathophysiological links between traumatic brain injury and post-traumatic headaches.

    PubMed

    Ruff, Robert L; Blake, Kayla

    2016-01-01

    This article reviews possible ways that traumatic brain injury (TBI) can induce migraine-type post-traumatic headaches (PTHs) in children, adults, civilians, and military personnel. Several cerebral alterations resulting from TBI can foster the development of PTH, including neuroinflammation that can activate neural systems associated with migraine. TBI can also compromise the intrinsic pain modulation system and this would increase the level of perceived pain associated with PTH. Depression and anxiety disorders, especially post-traumatic stress disorder (PTSD), are associated with TBI and these psychological conditions can directly intensify PTH. Additionally, depression and PTSD alter sleep and this will increase headache severity and foster the genesis of PTH. This article also reviews the anatomic loci of injury associated with TBI and notes the overlap between areas of injury associated with TBI and PTSD. PMID:27635228

  14. Pathophysiological links between traumatic brain injury and post-traumatic headaches

    PubMed Central

    Ruff, Robert L.; Blake, Kayla

    2016-01-01

    This article reviews possible ways that traumatic brain injury (TBI) can induce migraine-type post-traumatic headaches (PTHs) in children, adults, civilians, and military personnel. Several cerebral alterations resulting from TBI can foster the development of PTH, including neuroinflammation that can activate neural systems associated with migraine. TBI can also compromise the intrinsic pain modulation system and this would increase the level of perceived pain associated with PTH. Depression and anxiety disorders, especially post-traumatic stress disorder (PTSD), are associated with TBI and these psychological conditions can directly intensify PTH. Additionally, depression and PTSD alter sleep and this will increase headache severity and foster the genesis of PTH. This article also reviews the anatomic loci of injury associated with TBI and notes the overlap between areas of injury associated with TBI and PTSD. PMID:27635228

  15. Pathophysiological links between traumatic brain injury and post-traumatic headaches

    PubMed Central

    Ruff, Robert L.; Blake, Kayla

    2016-01-01

    This article reviews possible ways that traumatic brain injury (TBI) can induce migraine-type post-traumatic headaches (PTHs) in children, adults, civilians, and military personnel. Several cerebral alterations resulting from TBI can foster the development of PTH, including neuroinflammation that can activate neural systems associated with migraine. TBI can also compromise the intrinsic pain modulation system and this would increase the level of perceived pain associated with PTH. Depression and anxiety disorders, especially post-traumatic stress disorder (PTSD), are associated with TBI and these psychological conditions can directly intensify PTH. Additionally, depression and PTSD alter sleep and this will increase headache severity and foster the genesis of PTH. This article also reviews the anatomic loci of injury associated with TBI and notes the overlap between areas of injury associated with TBI and PTSD.

  16. Pathophysiological links between traumatic brain injury and post-traumatic headaches.

    PubMed

    Ruff, Robert L; Blake, Kayla

    2016-01-01

    This article reviews possible ways that traumatic brain injury (TBI) can induce migraine-type post-traumatic headaches (PTHs) in children, adults, civilians, and military personnel. Several cerebral alterations resulting from TBI can foster the development of PTH, including neuroinflammation that can activate neural systems associated with migraine. TBI can also compromise the intrinsic pain modulation system and this would increase the level of perceived pain associated with PTH. Depression and anxiety disorders, especially post-traumatic stress disorder (PTSD), are associated with TBI and these psychological conditions can directly intensify PTH. Additionally, depression and PTSD alter sleep and this will increase headache severity and foster the genesis of PTH. This article also reviews the anatomic loci of injury associated with TBI and notes the overlap between areas of injury associated with TBI and PTSD.

  17. Common Data Elements for Neuroimaging of Traumatic Brain Injury: Pediatric Considerations

    PubMed Central

    Holshouser, Barbara; Hunter, Jill V.; Tong, Karen

    2012-01-01

    Abstract As part of the Traumatic Brain Injury Common Data Elements project, a large-scale effort to define common data elements across a variety of domains, including neuroimaging, special considerations for pediatric patients were introduced. This article is an extension of that initial work, in which pediatric-specific pathoanatomical entities, technical considerations, interpretation paradigms, and safety considerations were reviewed. The goal of this review was to outline differences and specific information relevant to optimal performance and proper interpretation of neuroimaging in pediatric patients with traumatic brain injury. The long-range goal of this project is to facilitate data sharing as well as to provide critical infrastructure for potential clinical trials in this major public health area. PMID:21671798

  18. In-Vitro Approaches for Studying Blast-Induced Traumatic Brain Injury

    PubMed Central

    Chen, Yung Chia; Smith, Douglas H.

    2009-01-01

    Abstract Traumatic brain injury caused by explosive or blast events is currently divided into four phases: primary, secondary, tertiary, and quaternary blast injury. These phases of blast-induced traumatic brain injury (bTBI) are biomechanically distinct, and can be modeled in both in-vivo and in-vitro systems. The purpose of this review is to consider the mechanical phases of bTBI, how these phases are reproduced with in-vitro models, and to review findings from these models to assess how each phase of bTBI can be examined in more detail. Highlighted are some important gaps in the literature that may be addressed in the future to better identify the exact contributing mechanisms for bTBI. These in-vitro models, viewed in combination with in-vivo models and clinical studies, can be used to assess both the mechanisms and possible treatments for this type of trauma. PMID:19397424

  19. Driving after traumatic brain injury: evaluation and rehabilitation interventions

    PubMed Central

    Schultheis, Maria T.; Whipple, Elizabeth

    2014-01-01

    The ability to return to driving is a common goal for individuals who have sustained a traumatic brain injury. However, specific and empirically validated guidelines for clinicians who make the return-to-drive decision are sparse. In this article, we attempt to integrate previous findings on driving after brain injury and detail the cognitive, motor, and sensory factors necessary for safe driving that may be affected by brain injury. Various forms of evaluation (both in clinic and behind-the-wheel) are discussed, as well as driver retraining and modifications that may be necessary. PMID:25436178

  20. Neurological consequences of traumatic brain injuries in sports.

    PubMed

    Ling, Helen; Hardy, John; Zetterberg, Henrik

    2015-05-01

    Traumatic brain injury (TBI) is common in boxing and other contact sports. The long term irreversible and progressive aftermath of TBI in boxers depicted as punch drunk syndrome was described almost a century ago and is now widely referred as chronic traumatic encephalopathy (CTE). The short term sequelae of acute brain injury including subdural haematoma and catastrophic brain injury may lead to death, whereas mild TBI, or concussion, causes functional disturbance and axonal injury rather than gross structural brain damage. Following concussion, symptoms such as dizziness, nausea, reduced attention, amnesia and headache tend to develop acutely but usually resolve within a week or two. Severe concussion can also lead to loss of consciousness. Despite the transient nature of the clinical symptoms, functional neuroimaging, electrophysiological, neuropsychological and neurochemical assessments indicate that the disturbance of concussion takes over a month to return to baseline and neuropathological evaluation shows that concussion-induced axonopathy may persist for years. The developing brains in children and adolescents are more susceptible to concussion than adult brain. The mechanism by which acute TBI may lead to the neurodegenerative process of CTE associated with tau hyperphosphorylation and the development of neurofibrillary tangles (NFTs) remains speculative. Focal tau-positive NFTs and neurites in close proximity to focal axonal injury and foci of microhaemorrhage and the predilection of CTE-tau pathology for perivascular and subcortical regions suggest that acute TBI-related axonal injury, loss of microvascular integrity, breach of the blood brain barrier, resulting inflammatory cascade and microglia and astrocyte activation are likely to be the basis of the mechanistic link of TBI and CTE. This article provides an overview of the acute and long-term neurological consequences of TBI in sports. Clinical, neuropathological and the possible pathophysiological

  1. [Neuroendocrine dysfunctions and their consequences following traumatic brain injury].

    PubMed

    Czirják, Sándor; Rácz, Károly; Góth, Miklós

    2012-06-17

    Posttraumatic hypopituitarism is of major public health importance because it is more prevalent than previously thought. The prevalence of hypopituitarism in children with traumatic brain injury is unknown. Most cases of posttraumatic hypopituitarism remain undiagnosed and untreated in the clinical practice, and it may contribute to the severe morbidity seen in patients with traumatic brain injury. In the acute phase of brain injury, the diagnosis of adrenal insufficiency should not be missed. Determination of morning serum cortisol concentration is mandatory, because adrenal insufficiency can be life threatening. Morning serum cortisol lower than 200 nmol/L strongly suggests adrenal insufficiency. A complete hormonal investigation should be performed after one year of the trauma. Isolated growth hormone deficiency is the most common deficiency after traumatic brain injury. Sports-related chronic repetitive head trauma (because of boxing, kickboxing, football and ice hockey) may also result in hypopituitarism. Close co-operation between neurosurgeons, endocrinologists, rehabilitation physicians and representatives of other disciplines is important to provide better care for these patients. PMID:22695628

  2. Deferoxamine attenuates acute hydrocephalus after traumatic brain injury in rats.

    PubMed

    Zhao, Jinbing; Chen, Zhi; Xi, Guohua; Keep, Richard F; Hua, Ya

    2014-10-01

    Acute post-traumatic ventricular dilation and hydrocephalus are relatively frequent consequences of traumatic brain injury (TBI). Several recent studies have indicated that high iron levels in brain may relate to hydrocephalus development after intracranial hemorrhage. However, the role of iron in the development of post-traumatic hydrocephalus is still unclear. This study was to determine whether or not iron has a role in hydrocephalus development after TBI. TBI was induced by lateral fluid-percussion in male Sprague-Dawley rats. Some rats had intraventricular injection of iron. Acute hydrocephalus was measured by magnetic resonance T2-weighted imaging and brain hemorrhage was determined by T2* gradient-echo sequence imaging and brain hemoglobin levels. The effect of deferoxamine on TBI-induced hydrocephalus was examined. TBI resulted in acute hydrocephalus at 24 h (lateral ventricle volume: 24.1 ± 3.0 vs. 9.9 ± 0.2 mm(3) in sham group). Intraventricular injection of iron also caused hydrocephalus (25.7 ± 3.4 vs. 9.0 ± 0.6 mm(3) in saline group). Deferoxamine treatment attenuated TBI-induced hydrocephalus and heme oxygenase-1 upregulation. In conclusion, iron may contribute to acute hydrocephalus after TBI.

  3. [Neuroendocrine dysfunctions and their consequences following traumatic brain injury].

    PubMed

    Czirják, Sándor; Rácz, Károly; Góth, Miklós

    2012-06-17

    Posttraumatic hypopituitarism is of major public health importance because it is more prevalent than previously thought. The prevalence of hypopituitarism in children with traumatic brain injury is unknown. Most cases of posttraumatic hypopituitarism remain undiagnosed and untreated in the clinical practice, and it may contribute to the severe morbidity seen in patients with traumatic brain injury. In the acute phase of brain injury, the diagnosis of adrenal insufficiency should not be missed. Determination of morning serum cortisol concentration is mandatory, because adrenal insufficiency can be life threatening. Morning serum cortisol lower than 200 nmol/L strongly suggests adrenal insufficiency. A complete hormonal investigation should be performed after one year of the trauma. Isolated growth hormone deficiency is the most common deficiency after traumatic brain injury. Sports-related chronic repetitive head trauma (because of boxing, kickboxing, football and ice hockey) may also result in hypopituitarism. Close co-operation between neurosurgeons, endocrinologists, rehabilitation physicians and representatives of other disciplines is important to provide better care for these patients.

  4. Traumatic Brain Injury: Hope through Research

    MedlinePlus

    ... with TBI visited an emergency department [1] . This computer-generated graphic shows how, in 1848, a 3- ... carry electrical impulses). Like the wires in a computer, axons connect various areas of the brain to ...

  5. Linking Traumatic Brain Injury to Chronic Traumatic Encephalopathy: Identification of Potential Mechanisms Leading to Neurofibrillary Tangle Development

    PubMed Central

    Lucke-Wold, Brandon Peter; Turner, Ryan Coddington; Logsdon, Aric Flint; Bailes, Julian Edwin; Huber, Jason Delwyn

    2014-01-01

    Abstract Significant attention has recently been drawn to the potential link between head trauma and the development of neurodegenerative disease, namely chronic traumatic encephalopathy (CTE). The acute neurotrauma associated with sports-related concussions in athletes and blast-induced traumatic brain injury in soldiers elevates the risk for future development of chronic neurodegenerative diseases such as CTE. CTE is a progressive disease distinguished by characteristic tau neurofibrillary tangles (NFTs) and, occasionally, transactive response DNA binding protein 43 (TDP43) oligomers, both of which have a predilection for perivascular and subcortical areas near reactive astrocytes and microglia. The disease is currently only diagnosed postmortem by neuropathological identification of NFTs. A recent workshop sponsored by National Institute of Neurological Disorders and Stroke emphasized the need for premortem diagnosis, to better understand disease pathophysiology and to develop targeted treatments. In order to accomplish this objective, it is necessary to discover the mechanistic link between acute neurotrauma and the development of chronic neurodegenerative and neuropsychiatric disorders such as CTE. In this review, we briefly summarize what is currently known about CTE development and pathophysiology, and subsequently discuss injury-induced pathways that warrant further investigation. Understanding the mechanistic link between acute brain injury and chronic neurodegeneration will facilitate the development of appropriate diagnostic and therapeutic options for CTE and other related disorders. PMID:24499307

  6. The Role of Markers of Inflammation in Traumatic Brain Injury

    PubMed Central

    Woodcock, Thomas; Morganti-Kossmann, Maria Cristina

    2013-01-01

    Within minutes of a traumatic impact, a robust inflammatory response is elicited in the injured brain. The complexity of this post-traumatic squeal involves a cellular component, comprising the activation of resident glial cells, microglia, and astrocytes, and the infiltration of blood leukocytes. The second component regards the secretion immune mediators, which can be divided into the following sub-groups: the archetypal pro-inflammatory cytokines (Interleukin-1, Tumor Necrosis Factor, Interleukin-6), the anti-inflammatory cytokines (IL-4, Interleukin-10, and TGF-beta), and the chemotactic cytokines or chemokines, which specifically drive the accumulation of parenchymal and peripheral immune cells in the injured brain region. Such mechanisms have been demonstrated in animal models, mostly in rodents, as well as in human brain. Whilst the humoral immune response is particularly pronounced in the acute phase following Traumatic brain injury (TBI), the activation of glial cells seems to be a rather prolonged effect lasting for several months. The complex interaction of cytokines and cell types installs a network of events, which subsequently intersect with adjacent pathological cascades including oxidative stress, excitotoxicity, or reparative events including angiogenesis, scarring, and neurogenesis. It is well accepted that neuroinflammation is responsible of beneficial and detrimental effects, contributing to secondary brain damage but also facilitating neurorepair. Although such mediators are clear markers of immune activation, to what extent cytokines can be defined as diagnostic factors reflecting brain injury or as predictors of long term outcome needs to be further substantiated. In clinical studies some groups reported a proportional cytokine production in either the cerebrospinal fluid or intraparenchymal tissue with initial brain damage, mortality, or poor outcome scores. However, the validity of cytokines as biomarkers is not broadly accepted. This

  7. Aqueous Date Fruit Efficiency as Preventing Traumatic Brain Deterioration and Improving Pathological Parameters after Traumatic Brain Injury in Male Rats

    PubMed Central

    Badeli, Hamze; Shahrokhi, Nader; KhoshNazar, Mahdieosadat; Asadi-Shekaari, Majid; Shabani, Mohammad; Eftekhar Vaghefi, Hassan; Khaksari, Mohammad; Basiri, Mohsen

    2016-01-01

    Objective Following traumatic brain injury, disruption of blood-brain-barrier and consequent brain edema are critical events which might lead to increasing intracranial pressure (ICP), and nerve damage. The current study assessed the effects of aqueous date fruit extract (ADFE) on the aforementioned parameters. Materials and Methods In this experimental study, diffused traumatic brain injury (TBI) was generated in adult male rats using Marmarou’s method. Experimental groups include two pre-treatment (oral ADFE, 4 and 8 mL/kg for 14 days), vehicle (distilled water, for 14 days) and sham groups. Brain edema and neuronal injury were measured 72 hours after TBI. Veterinary coma scale (VCS) and ICP were determined at -1, 4, 24, 48 and 72 hours after TBI. Differences among multiple groups were assessed using ANOVA. Turkey’s test was employed for the ANOVA post-hoc analysis. The criterion of statistical significance was sign at P<0.05. Results Brain water content in ADFE-treated groups was decreased in comparison with the TBI+vehicle group. VCS at 24, 48 and 72 hours after TBI showed a significant increase in ADFE groups in comparison with the TBI+vehicle group. ICP at 24, 48 and 72 hours after TBI, was decreased in ADFE groups, compared to the TBI+vehicle. Brain edema, ICP and neuronal injury were also decreased in ADFE group, but VCS was increased following on TBI. Conclusion ADFE pre-treatment demonstrated an efficient method for preventing traumatic brain deterioration and improving pathological parameters after TBI.

  8. Aqueous Date Fruit Efficiency as Preventing Traumatic Brain Deterioration and Improving Pathological Parameters after Traumatic Brain Injury in Male Rats

    PubMed Central

    Badeli, Hamze; Shahrokhi, Nader; KhoshNazar, Mahdieosadat; Asadi-Shekaari, Majid; Shabani, Mohammad; Eftekhar Vaghefi, Hassan; Khaksari, Mohammad; Basiri, Mohsen

    2016-01-01

    Objective Following traumatic brain injury, disruption of blood-brain-barrier and consequent brain edema are critical events which might lead to increasing intracranial pressure (ICP), and nerve damage. The current study assessed the effects of aqueous date fruit extract (ADFE) on the aforementioned parameters. Materials and Methods In this experimental study, diffused traumatic brain injury (TBI) was generated in adult male rats using Marmarou’s method. Experimental groups include two pre-treatment (oral ADFE, 4 and 8 mL/kg for 14 days), vehicle (distilled water, for 14 days) and sham groups. Brain edema and neuronal injury were measured 72 hours after TBI. Veterinary coma scale (VCS) and ICP were determined at -1, 4, 24, 48 and 72 hours after TBI. Differences among multiple groups were assessed using ANOVA. Turkey’s test was employed for the ANOVA post-hoc analysis. The criterion of statistical significance was sign at P<0.05. Results Brain water content in ADFE-treated groups was decreased in comparison with the TBI+vehicle group. VCS at 24, 48 and 72 hours after TBI showed a significant increase in ADFE groups in comparison with the TBI+vehicle group. ICP at 24, 48 and 72 hours after TBI, was decreased in ADFE groups, compared to the TBI+vehicle. Brain edema, ICP and neuronal injury were also decreased in ADFE group, but VCS was increased following on TBI. Conclusion ADFE pre-treatment demonstrated an efficient method for preventing traumatic brain deterioration and improving pathological parameters after TBI. PMID:27602324

  9. Metacognitive monitoring in moderate and severe traumatic brain injury.

    PubMed

    Chiou, Kathy S; Carlson, Richard A; Arnett, Peter A; Cosentino, Stephanie A; Hillary, Frank G

    2011-07-01

    The ability to engage in self-reflective processes is a capacity that may be disrupted after neurological compromise; research to date has demonstrated that patients with traumatic brain injury (TBI) show reduced awareness of their deficits and functional ability compared to caretaker or clinician reports. Assessment of awareness of deficit, however, has been limited by the use of subjective measures (without comparison to actual performance) that are susceptible to report bias. This study used concurrent measurements from cognitive testing and confidence judgments about performance to investigate in-the-moment metacognitive experiences after moderate and severe traumatic brain injury. Deficits in metacognitive accuracy were found in adults with TBI for some but not all indices, suggesting that metacognition may not be a unitary construct. Findings also revealed that not all indices of executive functioning reliably predict metacognitive ability.

  10. Two approaches to behavior disorder after traumatic brain injury.

    PubMed

    Giles, Gordon Muir; Manchester, David

    2006-01-01

    A 3-stage model of intervention is used to contrast the philosophy and treatment practices of 2 behavioral approaches to behavior disorder following traumatic brain injury. The first referred to here as the Operant Neurobehavioral Approach developed from neuropsychology and learning theory. The second referred to as the Relational Neurobehavioral Approach builds on the nonaversive behavioral techniques of the Operant Neurobehavioral Approach. It also incorporates principles of motivational interviewing, places more overt emphasis on the therapeutic relationship, and targets staff attributions for aggression in staff training. The strengths and weaknesses of both approaches are discussed. It is suggested that the Relational Neurobehavioral Approach is more likely to engage and/or reengage clients with traumatic brain injury who are resistant to behavior change. Research implications are discussed including the need to measure the fidelity of all intervention variables.

  11. Neuropathology of mild traumatic brain injury: relationship to neuroimaging findings.

    PubMed

    Bigler, Erin D; Maxwell, William L

    2012-06-01

    Neuroimaging identified abnormalities associated with traumatic brain injury (TBI) are but gross indicators that reflect underlying trauma-induced neuropathology at the cellular level. This review examines how cellular pathology relates to neuroimaging findings with the objective of more closely relating how neuroimaging findings reveal underlying neuropathology. Throughout this review an attempt will be made to relate what is directly known from post-mortem microscopic and gross anatomical studies of TBI of all severity levels to the types of lesions and abnormalities observed in contemporary neuroimaging of TBI, with an emphasis on mild traumatic brain injury (mTBI). However, it is impossible to discuss the neuropathology of mTBI without discussing what occurs with more severe injury and viewing pathological changes on some continuum from the mildest to the most severe. Historical milestones in understanding the neuropathology of mTBI are reviewed along with implications for future directions in the examination of neuroimaging and neuropathological correlates of TBI.

  12. Combination Therapies for Traumatic Brain Injury: Prospective Considerations

    PubMed Central

    Hicks, Ramona

    2009-01-01

    Abstract Traumatic brain injury (TBI) initiates a cascade of numerous pathophysiological events that evolve over time. Despite the complexity of TBI, research aimed at therapy development has almost exclusively focused on single therapies, all of which have failed in multicenter clinical trials. Therefore, in February 2008 the National Institute of Neurological Disorders and Stroke, with support from the National Institute of Child Health and Development, the National Heart, Lung, and Blood Institute, and the Department of Veterans Affairs, convened a workshop to discuss the opportunities and challenges of testing combination therapies for TBI. Workshop participants included clinicians and scientists from a variety of disciplines, institutions, and agencies. The objectives of the workshop were to: (1) identify the most promising combinations of therapies for TBI; (2) identify challenges of testing combination therapies in clinical and pre-clinical studies; and (3) propose research methodologies and study designs to overcome these challenges. Several promising combination therapies were discussed, but no one combination was identified as being the most promising. Rather, the general recommendation was to combine agents with complementary targets and effects (e.g., mechanisms and time-points), rather than focusing on a single target with multiple agents. In addition, it was recommended that clinical management guidelines be carefully considered when designing pre-clinical studies for therapeutic development. To overcome the challenges of testing combination therapies it was recommended that statisticians and the U.S. Food and Drug Administration be included in early discussions of experimental design. Furthermore, it was agreed that an efficient and validated screening platform for candidate therapeutics, sensitive and clinically relevant biomarkers and outcome measures, and standardization and data sharing across centers would greatly facilitate the development of

  13. Manganese-Enhanced Magnetic Resonance Imaging of Traumatic Brain Injury

    PubMed Central

    Talley Watts, Lora; Shen, Qiang; Deng, Shengwen; Chemello, Jonathan

    2015-01-01

    Abstract Calcium dysfunction is involved in secondary traumatic brain injury (TBI). Manganese-enhanced MRI (MEMRI), in which the manganese ion acts as a calcium analog and a MRI contrast agent, was used to study rats subjected to a controlled cortical impact. Comparisons were made with conventional T2 MRI, sensorimotor behavior, and immunohistology. The major findings were: (1) Low-dose manganese (29 mg/kg) yielded excellent contrast with no negative effects on behavior scores relative to vehicle; (2) T1-weighted MEMRI was hyperintense in the impact area at 1–3 h, hypointense on day 2, and markedly hypointense with a hyperintense area surrounding the core on days 7 and/or 14, in contrast to the vehicle group, which did not show a biphasic profile; (3) in the hyperacute phase, the area of hyperintense T1-weighted MEMRI was larger than that of T2 MRI; (4) glial fibrillary acidic protein staining revealed that the MEMRI signal void in the impact core and the hyperintense area surrounding the core on day 7 and/or 14 corresponded to tissue cavitation and reactive gliosis, respectively; (5) T2 MRI showed little contrast in the impact core at 2 h, hyperintense on day 2 (indicative of vasogenic edema), hyperintense in some animals but pseudonormalized in others on day 7 and/or 14; (6) behavioral deficit peaked on day 2. We concluded that MEMRI detected early excitotoxic injury in the hyperacute phase, preceding vasogenic edema. In the subacute phase, MEMRI detected contrast consistent with tissue cavitation and reactive gliosis. MEMRI offers novel contrasts of biological processes that complement conventional MRI in TBI. PMID:25531419

  14. Emerging Imaging Tools for Use with Traumatic Brain Injury Research

    PubMed Central

    Wilde, Elisabeth A.; Tong, Karen A.; Holshouser, Barbara A.

    2012-01-01

    Abstract This article identifies emerging neuroimaging measures considered by the inter-agency Pediatric Traumatic Brain Injury (TBI) Neuroimaging Workgroup. This article attempts to address some of the potential uses of more advanced forms of imaging in TBI as well as highlight some of the current considerations and unresolved challenges of using them. We summarize emerging elements likely to gain more widespread use in the coming years, because of 1) their utility in diagnosis, prognosis, and understanding the natural course of degeneration or recovery following TBI, and potential for evaluating treatment strategies; 2) the ability of many centers to acquire these data with scanners and equipment that are readily available in existing clinical and research settings; and 3) advances in software that provide more automated, readily available, and cost-effective analysis methods for large scale data image analysis. These include multi-slice CT, volumetric MRI analysis, susceptibility-weighted imaging (SWI), diffusion tensor imaging (DTI), magnetization transfer imaging (MTI), arterial spin tag labeling (ASL), functional MRI (fMRI), including resting state and connectivity MRI, MR spectroscopy (MRS), and hyperpolarization scanning. However, we also include brief introductions to other specialized forms of advanced imaging that currently do require specialized equipment, for example, single photon emission computed tomography (SPECT), positron emission tomography (PET), encephalography (EEG), and magnetoencephalography (MEG)/magnetic source imaging (MSI). Finally, we identify some of the challenges that users of the emerging imaging CDEs may wish to consider, including quality control, performing multi-site and longitudinal imaging studies, and MR scanning in infants and children. PMID:21787167

  15. Sex Differences in Outcome after Mild Traumatic Brain Injury

    PubMed Central

    Blyth, Brian; Mookerjee, Sohug; He, Hua; McDermott, Michael P.

    2010-01-01

    Abstract The objective of this study was to estimate the independent association of sex with outcome after mild traumatic brain injury (mTBI). We performed an analysis of a subset of an established cohort involving 1425 mTBI patients presenting to an academic emergency department (ED). The associations between sex and three outcomes determined 3 months after the initial ED visit were examined: post-concussive symptom (PCS) score (0, 1–5, 6–16, and >16), the number of days to return of normal activities (0, 1–7, and >7), and the number of days of work missed (0, 1–7,and >7). Logistic regression analyses were used to determine the relationship between sex and each outcome after controlling for 12 relevant subject-level variables. Of the 1425 subjects, 643 (45.1%) were female and 782 (54.9%) were male. Three months after mTBI, males had significantly lower odds of being in a higher PCS score category (odds ratio [OR] 0.62, 95% confidence interval [CI]: 0.50, 0.78); this association appeared to be more prominent during child-bearing years for females. Males and females did not significantly differ with respect to the odds of poorer outcome as defined by the number of days to return of normal activities or the number of days of work missed. Female sex is associated with significantly higher odds of poor outcome after mTBI, as measured by PCS score, after control for appropriate confounders. The observed pattern of peak disability for females during the child-bearing years suggests disruption of endogenous estrogen or progesterone production. Attempts to better understand how mTBI affects production of these hormones acutely after injury and during the recovery period may shed light on the mechanism behind poorer outcome among females and putative therapeutic interventions. PMID:19938945

  16. Acute Gonadotroph and Somatotroph Hormonal Suppression after Traumatic Brain Injury

    PubMed Central

    Wagner, Justin; Dusick, Joshua R.; McArthur, David L.; Cohan, Pejman; Wang, Christina; Swerdloff, Ronald; Boscardin, W. John

    2010-01-01

    Abstract Hormonal dysfunction is a known consequence of moderate and severe traumatic brain injury (TBI). In this study we determined the incidence, time course, and clinical correlates of acute post-TBI gonadotroph and somatotroph dysfunction. Patients had daily measurement of serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, estradiol, growth hormone, and insulin-like growth factor-1 (IGF-1) for up to 10 days post-injury. Values below the fifth percentile of a healthy cohort were considered abnormal, as were non-measurable growth hormone (GH) values. Outcome measures were frequency and time course of hormonal suppression, injury characteristics, and Glasgow Outcome Scale (GOS) score. The cohort consisted of 101 patients (82% males; mean age 35 years; Glasgow Coma Scale [GCS] score ≤8 in 87%). In men, 100% had at least one low testosterone value, and 93% of all values were low; in premenopausal women, 43% had at least one low estradiol value, and 39% of all values were low. Non-measurable GH levels occurred in 38% of patients, while low IGF-1 levels were observed in 77% of patients, but tended to normalize within 10 days. Multivariate analysis revealed associations of younger age with low FSH and low IGF-1, acute anemia with low IGF-1, and older age and higher body mass index (BMI) with low GH. Hormonal suppression was not predictive of GOS score. These results indicate that within 10 days of complicated mild, moderate, and severe TBI, testosterone suppression occurs in all men and estrogen suppression occurs in over 40% of women. Transient somatotroph suppression occurs in over 75% of patients. Although this acute neuroendocrine dysfunction may not be TBI-specific, low gonadal steroids, IGF-1, and GH may be important given their putative neuroprotective functions. PMID:20214417

  17. Static and Dynamic Intrinsic Connectivity following Mild Traumatic Brain Injury

    PubMed Central

    Ling, Josef M.; Allen, Elena A.; Klimaj, Stefan D.; Yeo, Ronald A.; Hanlon, Faith M.

    2015-01-01

    Abstract Mild traumatic brain injury (mTBI) is the most common neurological disorder and is typically characterized by temporally limited cognitive impairment and emotional symptoms. Previous examinations of intrinsic resting state networks in mTBI have primarily focused on abnormalities in static functional connectivity, and deficits in dynamic functional connectivity have yet to be explored in this population. Resting-state data was collected on 48 semi-acute (mean=14 days post-injury) mTBI patients and 48 matched healthy controls. A high-dimensional independent component analysis (N=100) was utilized to parcellate intrinsic connectivity networks (ICN), with a priori hypotheses focusing on the default-mode network (DMN) and sub-cortical structures. Dynamic connectivity was characterized using a sliding window approach over 126 temporal epochs, with standard deviation serving as the primary outcome measure. Finally, distribution-corrected z-scores (DisCo-Z) were calculated to investigate changes in connectivity in a spatially invariant manner on a per-subject basis. Following appropriate correction for multiple comparisons, no significant group differences were evident on measures of static or dynamic connectivity within a priori ICN. Reduced (HC>mTBI patients) static connectivity was observed in the DMN at uncorrected (p<0.005) thresholds. Finally, a trend (p=0.07) for decreased dynamic connectivity in patients across all ICN was observed during spatially invariant analyses (DisCo-Z). In the semi-acute phase of recovery, mTBI was not reliably associated with abnormalities in static or dynamic functional connectivity within the DMN or sub-cortical structures. PMID:25318005

  18. A New Rabbit Model of Pediatric Traumatic Brain Injury

    PubMed Central

    Zhang, Zhi; Saraswati, Manda; Koehler, Raymond C.; Robertson, Courtney

    2015-01-01

    Abstract Traumatic brain injury (TBI) is a common cause of disability in childhood, resulting in numerous physical, behavioral, and cognitive sequelae, which can influence development through the lifespan. The mechanisms by which TBI influences normal development and maturation remain largely unknown. Pediatric rodent models of TBI often do not demonstrate the spectrum of motor and cognitive deficits seen in patients. To address this problem, we developed a New Zealand white rabbit model of pediatric TBI that better mimics the neurological injury seen after TBI in children. On postnatal Day 5-7 (P5-7), rabbits were injured by a controlled cortical impact (6-mm impactor tip; 5.5 m/sec, 2-mm depth, 50-msec duration). Rabbits from the same litter served as naïve (no injury) and sham (craniotomy alone) controls. Functional abilities and activity levels were measured 1 and 5 d after injury. Maturation level was monitored daily. We performed cognitive tests during P14-24 and sacrificed the animals at 1, 3, 7, and 21 d after injury to evaluate lesion volume and microglia. TBI kits exhibited delayed achievement of normal developmental milestones. They also demonstrated significant cognitive deficits, with lower percentage of correct alternation rate in the T-maze (n=9-15/group; p<0.001) and less discrimination between novel and old objects (p<0.001). Lesion volume increased from 16% at Day 3 to 30% at Day 7 after injury, indicating ongoing secondary injury. Activated microglia were noted at the injury site and also in white matter regions of the ipsilateral and contralateral hemispheres. The neurologic and histologic changes in this model are comparable to those reported clinically. Thus, this rabbit model provides a novel platform for evaluating neuroprotective therapies in pediatric TBI. PMID:25758339

  19. Comment: importance of cognitive reserve in traumatic brain injury.

    PubMed

    Bigler, Erin D

    2014-05-01

    The expectation for moderate to severe traumatic brain injury (TBI) is permanent damage and lasting deficits. However, in a multicenter investigation, Schneider et al.(1) show that by 1 year postinjury, one-fourth of patients with TBI achieve disability-free recovery (DFR), defined as a score of zero on the Disability Rating Scale. Of importance, cognitive reserve (CR) in the form of educational attainment was related to DFR.

  20. Cerebrovascular regulation, exercise, and mild traumatic brain injury

    PubMed Central

    Meehan, William P.; Iverson, Grant L.; Taylor, J. Andrew

    2014-01-01

    A substantial number of people who sustain a mild traumatic brain injury report persistent symptoms. Most common among these symptoms are headache, dizziness, and cognitive difficulties. One possible contributor to sustained symptoms may be compromised cerebrovascular regulation. In addition to injury-related cerebrovascular dysfunction, it is possible that prolonged rest after mild traumatic brain injury leads to deconditioning that may induce physiologic changes in cerebral blood flow control that contributes to persistent symptoms in some people. There is some evidence that exercise training may reduce symptoms perhaps because it engages an array of cerebrovascular regulatory mechanisms. Unfortunately, there is very little work on the degree of impairment in cerebrovascular control that may exist in patients with mild traumatic brain injury, and there are no published studies on the subacute phase of recovery from this injury. This review aims to integrate the current knowledge of cerebrovascular mechanisms that might underlie persistent symptoms and seeks to synthesize these data in the context of exploring aerobic exercise as a feasible intervention to treat the underlying pathophysiology. PMID:25274845

  1. Controlled cortical impact model for traumatic brain injury.

    PubMed

    Romine, Jennifer; Gao, Xiang; Chen, Jinhui

    2014-08-05

    Every year over a million Americans suffer a traumatic brain injury (TBI). Combined with the incidence of TBIs worldwide, the physical, emotional, social, and economical effects are staggering. Therefore, further research into the effects of TBI and effective treatments is necessary. The controlled cortical impact (CCI) model induces traumatic brain injuries ranging from mild to severe. This method uses a rigid impactor to deliver mechanical energy to an intact dura exposed following a craniectomy. Impact is made under precise parameters at a set velocity to achieve a pre-determined deformation depth. Although other TBI models, such as weight drop and fluid percussion, exist, CCI is more accurate, easier to control, and most importantly, produces traumatic brain injuries similar to those seen in humans. However, no TBI model is currently able to reproduce pathological changes identical to those seen in human patients. The CCI model allows investigation into the short-term and long-term effects of TBI, such as neuronal death, memory deficits, and cerebral edema, as well as potential therapeutic treatments for TBI.

  2. Affective state and community integration after traumatic brain injury.

    PubMed

    Juengst, Shannon B; Arenth, Patricia M; Raina, Ketki D; McCue, Michael; Skidmore, Elizabeth R

    2014-12-01

    Previous studies investigating the relationship between affective state and community integration have focused primarily on the influence of depression and anxiety. In addition, they have focused on frequency of participation in various activities, failing to address an individual's subjective satisfaction with participation. The purpose of this study was to examine how affective state contributes to frequency of participation and satisfaction with participation after traumatic brain injury among participants with and without a current major depressive episode. Sixty-four community-dwelling participants with a history of complicated mild-to-severe traumatic brain injury participated in this cross-sectional cohort study. High positive affect contributed significantly to frequency of participation (β = 0.401, P = 0.001), and both high positive affect and low negative affect significantly contributed to better satisfaction with participation (F2,61 = 13.63, P < 0.001). Further investigation to assess the direction of these relationships may better inform effective targets for intervention. These findings highlight the importance of assessing affective state after traumatic brain injury and incorporating a subjective measure of participation when considering community integration outcomes.

  3. Academic Placement after Traumatic Brain Injury.

    ERIC Educational Resources Information Center

    Donders, Jacques

    The acadmic placement of 87 children (ages 6 to 16 years) who had sustained brain injuries was determined within 1 year after initial psychological assessment. Forty-five children had returned full time to regular academic programs, 21 children received special education support for less than half of their classes, and 21 children were enrolled in…

  4. Acromegaly resolution after traumatic brain injury: a case report

    PubMed Central

    2014-01-01

    Introduction Anterior hypopituitarism is a common complication of head trauma, with a prevalence of 30% to 70% among long-term survivors. This is a much higher frequency than previously thought and suggests that most cases of post-traumatic hypopituitarism remain undiagnosed and untreated. Symptoms of hypopituitarism are very unspecific and very similar to those in traumatic brain injury patients in general, which makes hypopituitarism difficult to diagnose. The factors that predict the likelihood of developing hypopituitarism following traumatic brain injury remain poorly understood. The incidence of a specific hormone deficiency is variable, with growth hormone deficiency reported in 18% to 23% of cases. Case presentation A 23-year-old Hispanic man with a 2-year history of hypertension and diabetes presented with severe closed-head trauma producing diffuse axonal injury, subarachnoid hemorrhage and a brain concussion. A computed tomography scan showed a pituitary macroadenoma. The patient has clinical features of acromegaly and gigantism without other pituitary hyperfunctional manifestations or mass effect syndrome. A short-term post-traumatic laboratory test showed high levels of insulin like growth factor 1 and growth hormone, which are compatible with a growth hormone–producing pituitary tumor. At the third month post-trauma, the patient’s levels of insulin like growth factor 1 had decreased to low normal levels, with basal low levels of growth hormone. A glucose tolerance test completely suppressed the growth hormone, which confirmed resolution of acromegaly. An insulin tolerance test showed lack of stimulation of growth hormone and cortisol, demonstrating hypopituitarism of both axes. Conclusion Even though hypopituitarism is a frequent complication of traumatic brain injury, there are no reports in the literature, to the best of my knowledge, of patients with hyperfunctional pituitary adenomas, such as growth hormone–producing adenoma, that resolved

  5. Neurotransmitter Systems in a Mild Blast Traumatic Brain Injury Model: Catecholamines and Serotonin

    PubMed Central

    Arborelius, Ulf P.; Yoshitake, Takashi; Kehr, Jan; Hökfelt, Tomas; Risling, Mårten; Agoston, Denes

    2015-01-01

    Abstract Exposure to improvised explosive devices can result in a unique form of traumatic brain injury—blast-induced traumatic brain injury (bTBI). At the mild end of the spectrum (mild bTBI [mbTBI]), there are cognitive and mood disturbances. Similar symptoms have been observed in post-traumatic stress disorder caused by exposure to extreme psychological stress without physical injury. A role of the monoaminergic system in mood regulation and stress is well established but its involvement in mbTBI is not well understood. To address this gap, we used a rodent model of mbTBI and detected a decrease in immobility behavior in the forced swim test at 1 d post-exposure, coupled with an increase in climbing behavior, but not after 14 d or later, possibly indicating a transient increase in anxiety-like behavior. Using in situ hybridization, we found elevated messenger ribonucleic acid levels of both tyrosine hydroxylase and tryptophan hydroxylase 2 in the locus coeruleus and the dorsal raphe nucleus, respectively, as early as 2 h post-exposure. High-performance liquid chromatography analysis 1 d post-exposure primarily showed elevated noradrenaline levels in several forebrain regions. Taken together, we report that exposure to mild blast results in transient changes in both anxiety-like behavior and brain region–specific molecular changes, implicating the monoaminergic system in the pathobiology of mbTBI. PMID:25525686

  6. Glutamate and GABA imbalance following traumatic brain injury.

    PubMed

    Guerriero, Réjean M; Giza, Christopher C; Rotenberg, Alexander

    2015-05-01

    Traumatic brain injury (TBI) leads to multiple short- and long-term changes in neuronal circuits that ultimately conclude with an imbalance of cortical excitation and inhibition. Changes in neurotransmitter concentrations, receptor populations, and specific cell survival are important contributing factors. Many of these changes occur gradually, which may explain the vulnerability of the brain to multiple mild impacts, alterations in neuroplasticity, and delays in the presentation of posttraumatic epilepsy. In this review, we provide an overview of normal glutamate and GABA homeostasis and describe acute, subacute, and chronic changes that follow injury. We conclude by highlighting opportunities for therapeutic interventions in this paradigm. PMID:25796572

  7. Linguistic outcomes following traumatic brain injury in children.

    PubMed

    Ewing-Cobbs, Linda; Barnes, Marcia

    2002-09-01

    Recent studies of outcome after traumatic brain injury (TBI) emphasize the adverse effect of diffuse brain injury on linguistic development. This article reviews studies of lexical development, discourse processes, and reading in children and adolescents with TBI. The child's developmental level at the time of injury is related to the pattern of deficits. Young children who sustain severe TBI are particularly vulnerable to linguistic deficits at both lexical and discourse levels. TBI in older children and adolescents preferentially disrupts higher-order discourse functions. The contribution of deficits in fundamental processes, such as working memory and processing speed, to linguistic outcomes requires further investigation.

  8. Linguistic outcomes following traumatic brain injury in children.

    PubMed

    Ewing-Cobbs, Linda; Barnes, Marcia

    2002-09-01

    Recent studies of outcome after traumatic brain injury (TBI) emphasize the adverse effect of diffuse brain injury on linguistic development. This article reviews studies of lexical development, discourse processes, and reading in children and adolescents with TBI. The child's developmental level at the time of injury is related to the pattern of deficits. Young children who sustain severe TBI are particularly vulnerable to linguistic deficits at both lexical and discourse levels. TBI in older children and adolescents preferentially disrupts higher-order discourse functions. The contribution of deficits in fundamental processes, such as working memory and processing speed, to linguistic outcomes requires further investigation. PMID:12350042

  9. Current pre-hospital traumatic brain injury management in China

    PubMed Central

    Kou, Kou; Hou, Xiang-yu; Sun, Jian-dong; Chu, Kevin

    2014-01-01

    BACKGROUND: Traumatic brain injury (TBI) is associated with most trauma-related deaths. Secondary brain injury is the leading cause of in-hospital deaths after traumatic brain injury. By early prevention and slowing of the initial pathophysiological mechanism of secondary brain injury, pre-hospital service can significantly reduce case-fatality rates of TBI. In China, the incidence of TBI is increasing and the proportion of severe TBI is much higher than that in other countries. The objective of this paper is to review the pre-hospital management of TBI in China. DATA SOURCES: A literature search was conducted in January 2014 using the China National Knowledge Infrastructure (CNKI). Articles on the assessment and treatment of TBI in pre-hospital settings practiced by Chinese doctors were identified. The information on the assessment and treatment of hypoxemia, hypotension, and brain herniation was extracted from the identified articles. RESULTS: Of the 471 articles identified, 65 met the selection criteria. The existing literature indicated that current practices of pre-hospital TBI management in China were sub-optimal and varied considerably across different regions. CONCLUSION: Since pre-hospital care is the weakest part of Chinese emergency care, appropriate training programs on pre-hospital TBI management are urgently needed in China. PMID:25548596

  10. Lateral (Parasagittal) Fluid Percussion Model of Traumatic Brain Injury.

    PubMed

    Van, Ken C; Lyeth, Bruce G

    2016-01-01

    Fluid percussion was first conceptualized in the 1940s and has evolved into one of the leading laboratory methods for studying experimental traumatic brain injury (TBI). Over the decades, fluid percussion has been used in numerous species and today is predominantly applied to the rat. The fluid percussion technique rapidly injects a small volume of fluid, such as isotonic saline, through a circular craniotomy onto the intact dura overlying the brain cortex. In brief, the methods involve surgical production of a circular craniotomy, attachment of a fluid-filled conduit between the dura overlying the cortex and the outlet port of the fluid percussion device. A fluid pulse is then generated by the free-fall of a pendulum striking a piston on the fluid-filled cylinder of the device. The fluid enters the cranium, producing a compression and displacement of the brain parenchyma resulting in a sharp, high magnitude elevation of intracranial pressure that is propagated diffusely through the brain. This results in an immediate and transient period of traumatic unconsciousness as well as a combination of focal and diffuse damage to the brain, which is evident upon histological and behavioral analysis. Numerous studies have demonstrated that the rat fluid percussion model reproduces a wide range of pathological features associated with human TBI. PMID:27604722

  11. BDNF Polymorphism Predicts General Intelligence after Penetrating Traumatic Brain Injury

    PubMed Central

    Rostami, Elham; Krueger, Frank; Zoubak, Serguei; Dal Monte, Olga; Raymont, Vanessa; Pardini, Matteo; Hodgkinson, Colin A.; Goldman, David; Risling, Mårten; Grafman, Jordan

    2011-01-01

    Neuronal plasticity is a fundamental factor in cognitive outcome following traumatic brain injury. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, plays an important role in this process. While there are many ways to measure cognitive outcome, general cognitive intelligence is a strong predictor of everyday decision-making, occupational attainment, social mobility and job performance. Thus it is an excellent measure of cognitive outcome following traumatic brain injury (TBI). Although the importance of the single-nucleotide polymorphisms polymorphism on cognitive function has been previously addressed, its role in recovery of general intelligence following TBI is unknown. We genotyped male Caucasian Vietnam combat veterans with focal penetrating TBI (pTBI) (n = 109) and non-head injured controls (n = 38) for 7 BDNF single-nucleotide polymorphisms. Subjects were administrated the Armed Forces Qualification Test (AFQT) at three different time periods: pre-injury on induction into the military, Phase II (10–15 years post-injury, and Phase III (30–35 years post-injury). Two single-nucleotide polymorphisms, rs7124442 and rs1519480, were significantly associated with post-injury recovery of general cognitive intelligence with the most pronounced effect at the Phase II time point, indicating lesion-induced plasticity. The genotypes accounted for 5% of the variance of the AFQT scores, independently of other significant predictors such as pre-injury intelligence and percentage of brain volume loss. These data indicate that genetic variations in BDNF play a significant role in lesion-induced recovery following pTBI. Identifying the underlying mechanism of this brain-derived neurotrophic factor effect could provide insight into an important aspect of post-traumatic cognitive recovery. PMID:22087305

  12. Art Therapy for Individuals with Traumatic Brain Injury: A Comprehensive Neurorehabilitation-Informed Approach to Treatment

    ERIC Educational Resources Information Center

    Kline, Tori

    2016-01-01

    I describe an approach to art therapy treatment for survivors of traumatic brain injury developed at a rehabilitation facility for adults that serves inpatient, outpatient, and long-term residential clients. This approach is based on a review of the literature on traumatic brain injury, comprehensive neurorehabilitation, brain plasticity, and art…

  13. Epidemiology of mild traumatic brain injury and neurodegenerative disease

    PubMed Central

    Gardner, Raquel C.; Yaffe, Kristine

    2015-01-01

    Every year an estimated 42 million people worldwide suffer a mild traumatic brain injury (MTBI) or concussion. More severe traumatic brain injury (TBI) is a well-established risk factor for a variety of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS). Recently, large epidemiological studies have additionally identified MTBI as a risk factor for dementia. The role of MTBI in risk of PD or ALS is less well established. Repetitive MTBI and repetitive sub-concussive head trauma has been linked to increased risk for a variety of neurodegenerative diseases including chronic traumatic encephalopathy (CTE). CTE is a unique neurodegenerative tauopathy first described in boxers but more recently described in a variety of contact sport athletes, military veterans, and civilians exposed to repetitive MTBI. Studies of repetitive MTBI and CTE have been limited by referral bias, lack of consensus clinical criteria for CTE, challenges of quantifying MTBI exposure, and potential for confounding. The prevalence of CTE is unknown and the amount of MTBI or sub-concussive trauma exposure necessary to produce CTE is unclear. This review will summarize the current literature regarding the epidemiology of MTBI, post-TBI dementia and Parkinson's disease, and CTE while highlighting methodological challenges and critical future directions of research in this field. PMID:25748121

  14. Near-Infrared Spectroscopy in the Monitoring of Adult Traumatic Brain Injury: A Review

    PubMed Central

    Su, Zhangjie; Clancy, Michael T.; Lucas, Samuel J. E.; Dehghani, Hamid; Logan, Ann; Belli, Antonio

    2015-01-01

    Abstract Cerebral near-infrared spectroscopy (NIRS) has long represented an exciting prospect for the noninvasive monitoring of cerebral tissue oxygenation and perfusion in the context of traumatic brain injury (TBI), although uncertainty still exists regarding the reliability of this technology specifically within this field. We have undertaken a review of the existing literature relating to the application of NIRS within TBI. We discuss current “state-of-the-art” NIRS monitoring, provide a brief background of the technology, and discuss the evidence regarding the ability of NIRS to substitute for established invasive monitoring in TBI. PMID:25603012

  15. [Guidelines for the management of severe traumatic brain injury. Part 3. Surgical management of severe traumatic brain injury (Options)].

    PubMed

    Potapov, A A; Krylov, V V; Gavrilov, A G; Kravchuk, A D; Likhterman, L B; Petrikov, S S; Talypov, A E; Zakharova, N E; Solodov, A A

    2016-01-01

    Traumatic brain injury (TBI) is one of the main causes of mortality and severe disability in young and middle age patients. Patients with severe TBI, who are in coma, are of particular concern. Adequate diagnosis of primary brain injuries and timely prevention and treatment of secondary injury mechanisms markedly affect the possibility of reducing mortality and severe disability. The present guidelines are based on the authors' experience in developing international and national recommendations for the diagnosis and treatment of mild TBI, penetrating gunshot wounds of the skull and brain, severe TBI, and severe consequences of brain injury, including a vegetative state. In addition, we used the materials of international and national guidelines for the diagnosis, intensive care, and surgical treatment of severe TBI, which were published in recent years. The proposed recommendations for surgical treatment of severe TBI in adults are addressed primarily to neurosurgeons, neurologists, neuroradiologists, anesthesiologists, and intensivists who are routinely involved in treating these patients.

  16. [Guidelines for the management of severe traumatic brain injury. Part 3. Surgical management of severe traumatic brain injury (Options)].

    PubMed

    Potapov, A A; Krylov, V V; Gavrilov, A G; Kravchuk, A D; Likhterman, L B; Petrikov, S S; Talypov, A E; Zakharova, N E; Solodov, A A

    2016-01-01

    Traumatic brain injury (TBI) is one of the main causes of mortality and severe disability in young and middle age patients. Patients with severe TBI, who are in coma, are of particular concern. Adequate diagnosis of primary brain injuries and timely prevention and treatment of secondary injury mechanisms markedly affect the possibility of reducing mortality and severe disability. The present guidelines are based on the authors' experience in developing international and national recommendations for the diagnosis and treatment of mild TBI, penetrating gunshot wounds of the skull and brain, severe TBI, and severe consequences of brain injury, including a vegetative state. In addition, we used the materials of international and national guidelines for the diagnosis, intensive care, and surgical treatment of severe TBI, which were published in recent years. The proposed recommendations for surgical treatment of severe TBI in adults are addressed primarily to neurosurgeons, neurologists, neuroradiologists, anesthesiologists, and intensivists who are routinely involved in treating these patients. PMID:27070263

  17. Brain MRI volumetry in a single patient with mild traumatic brain injury.

    PubMed

    Ross, David E; Castelvecchi, Cody; Ochs, Alfred L

    2013-01-01

    This letter to the editor describes the case of a 42 year old man with mild traumatic brain injury and multiple neuropsychiatric symptoms which persisted for a few years after the injury. Initial CT scans and MRI scans of the brain showed no signs of atrophy. Brain volume was measured using NeuroQuant®, an FDA-approved, commercially available software method. Volumetric cross-sectional (one point in time) analysis also showed no atrophy. However, volumetric longitudinal (two points in time) analysis showed progressive atrophy in several brain regions. This case illustrated in a single patient the principle discovered in multiple previous group studies, namely that the longitudinal design is more powerful than the cross-sectional design for finding atrophy in patients with traumatic brain injury.

  18. Recovery from Mild Traumatic Brain Injury in Previously Healthy Adults.

    PubMed

    Losoi, Heidi; Silverberg, Noah D; Wäljas, Minna; Turunen, Senni; Rosti-Otajärvi, Eija; Helminen, Mika; Luoto, Teemu M; Julkunen, Juhani; Öhman, Juha; Iverson, Grant L

    2016-04-15

    This prospective longitudinal study reports recovery from mild traumatic brain injury (MTBI) across multiple domains in a carefully selected consecutive sample of 74 previously healthy adults. The patients with MTBI and 40 orthopedic controls (i.e., ankle injuries) completed assessments at 1, 6, and 12 months after injury. Outcome measures included cognition, post-concussion symptoms, depression, traumatic stress, quality of life, satisfaction with life, resilience, and return to work. Patients with MTBI reported more post-concussion symptoms and fatigue than the controls at the beginning of recovery, but by 6 months after injury, did not differ as a group from nonhead injury trauma controls on cognition, fatigue, or mental health, and by 12 months, their level of post-concussion symptoms and quality of life was similar to that of controls. Almost all (96%) patients with MTBI returned to work/normal activities (RTW) within the follow-up of 1 year. A subgroup of those with MTBIs and controls reported mild post-concussion-like symptoms at 1 year. A large percentage of the subgroup who had persistent symptoms had a modifiable psychological risk factor at 1 month (i.e., depression, traumatic stress, and/or low resilience), and at 6 months, they had greater post-concussion symptoms, fatigue, insomnia, traumatic stress, and depression, and worse quality of life. All of the control subjects who had mild post-concussion-like symptoms at 12 months also had a mental health problem (i.e., depression, traumatic stress, or both). This illustrates the importance of providing evidence-supported treatment and rehabilitation services early in the recovery period.

  19. Blast Exposure Induces Post-Traumatic Stress Disorder-Related Traits in a Rat Model of Mild Traumatic Brain Injury

    PubMed Central

    Dorr, Nathan P.; De Gasperi, Rita; Gama Sosa, Miguel A.; Shaughness, Michael C.; Maudlin-Jeronimo, Eric; Hall, Aaron A.; McCarron, Richard M.; Ahlers, Stephen T.

    2012-01-01

    Abstract Blast related traumatic brain injury (TBI) has been a major cause of injury in the wars in Iraq and Afghanistan. A striking feature of the mild TBI (mTBI) cases has been the prominent association with post-traumatic stress disorder (PTSD). However, because of the overlapping symptoms, distinction between the two disorders has been difficult. We studied a rat model of mTBI in which adult male rats were exposed to repetitive blast injury while under anesthesia. Blast exposure induced a variety of PTSD-related behavioral traits that were present many months after the blast exposure, including increased anxiety, enhanced contextual fear conditioning, and an altered response in a predator scent assay. We also found elevation in the amygdala of the protein stathmin 1, which is known to influence the generation of fear responses. Because the blast overpressure injuries occurred while animals were under general anesthesia, our results suggest that a blast-related mTBI exposure can, in the absence of any psychological stressor, induce PTSD-related traits that are chronic and persistent. These studies have implications for understanding the relationship of PTSD to mTBI in the population of veterans returning from the wars in Iraq and Afghanistan. PMID:22780833

  20. The Effects of Mild Traumatic Brain Injury, Post-Traumatic Stress Disorder, and Combined Mild Traumatic Brain Injury/Post-Traumatic Stress Disorder on Returning Veterans.

    PubMed

    Combs, Hannah L; Berry, David T R; Pape, Theresa; Babcock-Parziale, Judith; Smith, Bridget; Schleenbaker, Randal; Shandera-Ochsner, Anne; Harp, Jordan P; High, Walter M

    2015-07-01

    United States veterans of the Iraqi (Operation Iraqi Freedom [OIF]) and Afghanistan (Operation Enduring Freedom [OEF]) conflicts have frequently returned from deployment after sustaining mild traumatic brain injury (mTBI) and enduring stressful events resulting in post-traumatic stress disorder (PTSD). A large number of returning service members have been diagnosed with both a history of mTBI and current PTSD. Substantial literature exists on the neuropsychological factors associated with mTBI and PTSD occurring separately; far less research has explored the combined effects of PTSD and mTBI. The current study employed neuropsychological and psychological measures in a sample of 251 OIF/OEF veterans to determine whether participants with a history of mTBI and current PTSD (mTBI+PTSD) have poorer cognitive and psychological outcomes than participants with mTBI only (mTBI-o), PTSD only (PTSD-o), or veteran controls (VC), when groups are comparable on intelligence quotient, education, and age. The mTBI+PTSD group performed more poorly than VC, mTBI-o, and PTSD-o groups on several neuropsychological measures. Effect size comparisons suggest small deleterious effects for mTBI-o on measures of processing speed and visual attention and small effects for PTSD-o on measures of verbal memory, with moderate effects for mTBI+PTSD on the same variables. Additionally, the mTBI+PTSD group was significantly more psychologically distressed than the PTSD-o group, and PTSD-o group was more distressed than VC and mTBI-o groups. These findings suggest that veterans with mTBI+PTSD perform significantly lower on neuropsychological and psychiatric measures than veterans with mTBI-o or PTSD-o. The results also raise the possibility of mild but persisting cognitive changes following mTBI sustained during deployment.

  1. The Effects of Mild Traumatic Brain Injury, Post-Traumatic Stress Disorder, and Combined Mild Traumatic Brain Injury/Post-Traumatic Stress Disorder on Returning Veterans.

    PubMed

    Combs, Hannah L; Berry, David T R; Pape, Theresa; Babcock-Parziale, Judith; Smith, Bridget; Schleenbaker, Randal; Shandera-Ochsner, Anne; Harp, Jordan P; High, Walter M

    2015-07-01

    United States veterans of the Iraqi (Operation Iraqi Freedom [OIF]) and Afghanistan (Operation Enduring Freedom [OEF]) conflicts have frequently returned from deployment after sustaining mild traumatic brain injury (mTBI) and enduring stressful events resulting in post-traumatic stress disorder (PTSD). A large number of returning service members have been diagnosed with both a history of mTBI and current PTSD. Substantial literature exists on the neuropsychological factors associated with mTBI and PTSD occurring separately; far less research has explored the combined effects of PTSD and mTBI. The current study employed neuropsychological and psychological measures in a sample of 251 OIF/OEF veterans to determine whether participants with a history of mTBI and current PTSD (mTBI+PTSD) have poorer cognitive and psychological outcomes than participants with mTBI only (mTBI-o), PTSD only (PTSD-o), or veteran controls (VC), when groups are comparable on intelligence quotient, education, and age. The mTBI+PTSD group performed more poorly than VC, mTBI-o, and PTSD-o groups on several neuropsychological measures. Effect size comparisons suggest small deleterious effects for mTBI-o on measures of processing speed and visual attention and small effects for PTSD-o on measures of verbal memory, with moderate effects for mTBI+PTSD on the same variables. Additionally, the mTBI+PTSD group was significantly more psychologically distressed than the PTSD-o group, and PTSD-o group was more distressed than VC and mTBI-o groups. These findings suggest that veterans with mTBI+PTSD perform significantly lower on neuropsychological and psychiatric measures than veterans with mTBI-o or PTSD-o. The results also raise the possibility of mild but persisting cognitive changes following mTBI sustained during deployment. PMID:25350012

  2. Traumatic Brain Injury-Induced Ependymal Ciliary Loss Decreases Cerebral Spinal Fluid Flow

    PubMed Central

    Xiong, Guoxiang; Elkind, Jaclynn A.; Kundu, Suhali; Smith, Colin J.; Antunes, Marcelo B.; Tamashiro, Edwin; Kofonow, Jennifer M.; Mitala, Christina. M.; Stein, Sherman C.; Grady, M. Sean; Einhorn, Eugene; Cohen, Noam A.

    2014-01-01

    Abstract Traumatic brain injury (TBI) afflicts up to 2 million people annually in the United States and is the primary cause of death and disability in young adults and children. Previous TBI studies have focused predominantly on the morphological, biochemical, and functional alterations of gray matter structures, such as the hippocampus. However, little attention has been given to the brain ventricular system, despite the fact that altered ventricular function is known to occur in brain pathologies. In the present study, we investigated anatomical and functional alterations to mouse ventricular cilia that result from mild TBI. We demonstrate that TBI causes a dramatic decrease in cilia. Further, using a particle tracking technique, we demonstrate that cerebrospinal fluid flow is diminished, thus potentially negatively affecting waste and nutrient exchange. Interestingly, injury-induced ventricular system pathology resolves completely by 30 days after injury as ependymal cell ciliogenesis restores cilia density to uninjured levels in the affected lateral ventricle. PMID:24749541

  3. Apelin-13 as a novel target for intervention in secondary injury after traumatic brain injury.

    PubMed

    Bao, Hai-Jun; Qiu, Hai-Yang; Kuai, Jin-Xia; Song, Cheng-Jie; Wang, Shao-Xian; Wang, Chao-Qun; Peng, Hua-Bin; Han, Wen-Can; Wu, Yong-Ping

    2016-07-01

    The adipocytokine, apelin-13, is an abundantly expressed peptide in the nervous system. Apelin-13 protects the brain against ischemia/reperfusion injury and attenuates traumatic brain injury by suppressing autophagy. However, secondary apelin-13 effects on traumatic brain injury-induced neural cell death and blood-brain barrier integrity are still not clear. Here, we found that apelin-13 significantly decreases cerebral water content, mitigates blood-brain barrier destruction, reduces aquaporin-4 expression, diminishes caspase-3 and Bax expression in the cerebral cortex and hippocampus, and reduces apoptosis. These results show that apelin-13 attenuates secondary injury after traumatic brain injury and exerts a neuroprotective effect. PMID:27630697

  4. Apelin-13 as a novel target for intervention in secondary injury after traumatic brain injury

    PubMed Central

    Bao, Hai-jun; Qiu, Hai-yang; Kuai, Jin-xia; Song, Cheng-jie; Wang, Shao-xian; Wang, Chao-qun; Peng, Hua-bin; Han, Wen-can; Wu, Yong-ping

    2016-01-01

    The adipocytokine, apelin-13, is an abundantly expressed peptide in the nervous system. Apelin-13 protects the brain against ischemia/reperfusion injury and attenuates traumatic brain injury by suppressing autophagy. However, secondary apelin-13 effects on traumatic brain injury-induced neural cell death and blood-brain barrier integrity are still not clear. Here, we found that apelin-13 significantly decreases cerebral water content, mitigates blood-brain barrier destruction, reduces aquaporin-4 expression, diminishes caspase-3 and Bax expression in the cerebral cortex and hippocampus, and reduces apoptosis. These results show that apelin-13 attenuates secondary injury after traumatic brain injury and exerts a neuroprotective effect.

  5. Apelin-13 as a novel target for intervention in secondary injury after traumatic brain injury

    PubMed Central

    Bao, Hai-jun; Qiu, Hai-yang; Kuai, Jin-xia; Song, Cheng-jie; Wang, Shao-xian; Wang, Chao-qun; Peng, Hua-bin; Han, Wen-can; Wu, Yong-ping

    2016-01-01

    The adipocytokine, apelin-13, is an abundantly expressed peptide in the nervous system. Apelin-13 protects the brain against ischemia/reperfusion injury and attenuates traumatic brain injury by suppressing autophagy. However, secondary apelin-13 effects on traumatic brain injury-induced neural cell death and blood-brain barrier integrity are still not clear. Here, we found that apelin-13 significantly decreases cerebral water content, mitigates blood-brain barrier destruction, reduces aquaporin-4 expression, diminishes caspase-3 and Bax expression in the cerebral cortex and hippocampus, and reduces apoptosis. These results show that apelin-13 attenuates secondary injury after traumatic brain injury and exerts a neuroprotective effect. PMID:27630697

  6. The military's approach to traumatic brain injury and post-traumatic stress disorder

    NASA Astrophysics Data System (ADS)

    Ling, Geoffrey S. F.; Grimes, Jamie; Ecklund, James M.

    2014-06-01

    Traumatic brain injury (TBI) and Post Traumatic Stress Disorder (PTSD) are common conditions. In Iraq and Afghanistan, explosive blast related TBI became prominent among US service members but the vast majority of TBI was still due to typical causes such as falls and sporting events. PTS has long been a focus of the US military mental health providers. Combat Stress Teams have been integral to forward deployed units since the beginning of the Global War on Terror. Military medical management of disease and injury follows standard of care clinical practice guidelines (CPG) established by civilian counterparts. However, when civilian CPGs do not exist or are not applicable to the military environment, new practice standards are created. Such is the case for mild TBI. In 2009, the VA-DoD CPG for management of mild TBI/concussion was published and a system-wide clinical care program for mild TBI/concussion was introduced. This was the first large scale effort on an entire medical care system to address all severities of TBI in a comprehensive organized way. In 2010, the VA-DoD CPG for management of PTSD was published. Nevertheless, both TBI and PTS are still incompletely understood. Investment in terms of money and effort has been committed by the DoD to their study. The Defense and Veterans Brain Injury Center, National Intrepid Center of Excellence and the Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury are prominent examples of this effort. These are just beginnings, a work in progress ready to leverage advances made scientifically and always striving to provide the very best care to its military beneficiaries.

  7. Midline (Central) Fluid Percussion Model of Traumatic Brain Injury.

    PubMed

    Rowe, Rachel K; Griffiths, Daniel R; Lifshitz, Jonathan

    2016-01-01

    Research models of traumatic brain injury (TBI) hold significant validity towards the human condition, with each model replicating a subset of clinical features and symptoms. After 30 years of characterization and implementation, fluid percussion injury (FPI) is firmly recognized as a clinically relevant model of TBI, encompassing concussion through severe injury. The midline variation of FPI may best represent mild and diffuse clinical brain injury, because of the acute behavioral deficits, the late onset of subtle behavioral morbidities, and the absence of gross histopathology. This chapter outlines the procedures for midline (diffuse) FPI in adult male rats and mice. With these procedures, it becomes possible to generate brain-injured laboratory animals for studies of injury-induced pathophysiology and behavioral deficits, for which rational therapeutic interventions can be implemented. PMID:27604721

  8. Magnetic Resonance Imaging in Experimental Traumatic Brain Injury.

    PubMed

    Shen, Qiang; Watts, Lora Tally; Li, Wei; Duong, Timothy Q

    2016-01-01

    Traumatic brain injury (TBI) is a leading cause of death and disability in the USA. Common causes of TBI include falls, violence, injuries from wars, and vehicular and sporting accidents. The initial direct mechanical damage in TBI is followed by progressive secondary injuries such as brain swelling, perturbed cerebral blood flow (CBF), abnormal cerebrovascular reactivity (CR), metabolic dysfunction, blood-brain-barrier disruption, inflammation, oxidative stress, and excitotoxicity, among others. Magnetic resonance imaging (MRI) offers the means to noninvasively probe many of these secondary injuries. MRI has been used to image anatomical, physiological, and functional changes associated with TBI in a longitudinal manner. This chapter describes controlled cortical impact (CCI) TBI surgical procedures, a few common MRI protocols used in TBI imaging, and, finally, image analysis pertaining to experimental TBI imaging in rats. PMID:27604743

  9. Traumatic brain injury and obesity induce persistent central insulin resistance.

    PubMed

    Karelina, Kate; Sarac, Benjamin; Freeman, Lindsey M; Gaier, Kristopher R; Weil, Zachary M

    2016-04-01

    Traumatic brain injury (TBI)-induced impairments in cerebral energy metabolism impede tissue repair and contribute to delayed functional recovery. Moreover, the transient alteration in brain glucose utilization corresponds to a period of increased vulnerability to the negative effects of a subsequent TBI. In order to better understand the factors contributing to TBI-induced central metabolic dysfunction, we examined the effect of single and repeated TBIs on brain insulin signalling. Here we show that TBI induced acute brain insulin resistance, which resolved within 7 days following a single injury but persisted until 28 days following repeated injuries. Obesity, which causes brain insulin resistance and neuroinflammation, exacerbated the consequences of TBI. Obese mice that underwent a TBI exhibited a prolonged reduction of Akt (also known as protein kinase B) signalling, exacerbated neuroinflammation (microglial activation), learning and memory deficits, and anxiety-like behaviours. Taken together, the transient changes in brain insulin sensitivity following TBI suggest a reduced capacity of the injured brain to respond to the neuroprotective and anti-inflammatory actions of insulin and Akt signalling, and thus may be a contributing factor for the damaging neuroinflammation and long-lasting deficits that occur following TBI. PMID:26833850

  10. Considerations for animal models of blast-related traumatic brain injury and chronic traumatic encephalopathy

    PubMed Central

    2014-01-01

    The association of military blast exposure and brain injury was first appreciated in World War I as commotio cerebri, and later as shell shock. Similar injuries sustained in modern military conflicts are now classified as mild traumatic brain injury (TBI). Recent research has yielded new insights into the mechanisms by which blast exposure leads to acute brain injury and chronic sequelae, including postconcussive syndrome, post-traumatic stress disorder, post-traumatic headache, and chronic traumatic encephalopathy, a tau protein neurodegenerative disease. Impediments to delivery of effective medical care for individuals affected by blast-related TBI include: poor insight into the heterogeneity of neurological insults induced by blast exposure; limited understanding of the mechanisms by which blast exposure injures the brain and triggers sequelae; failure to appreciate interactive injuries that affect frontal lobe function, pituitary regulation, and neurovegetative homeostasis; unknown influence of genetic risk factors, prior trauma, and comorbidities; absence of validated diagnostic criteria and clinical nosology that differentiate clinical endophenotypes; and lack of empirical evidence to guide medical management and therapeutic intervention. While clinicopathological analysis can provide evidence of correlative association, experimental use of animal models remains the primary tool for establishing causal mechanisms of disease. However, the TBI field is confronted by a welter of animal models with varying clinical relevance, thereby impeding scientific coherence and hindering translational progress. Animal models of blast TBI will be far more translationally useful if experimental emphasis focuses on accurate reproduction of clinically relevant endpoints (output) rather than scaled replication of idealized blast shockwaves (input). The utility of an animal model is dependent on the degree to which the model recapitulates pathophysiological mechanisms

  11. Male pituitary-gonadal dysfunction following severe traumatic brain injury.

    PubMed

    Lee, S C; Zasler, N D; Kreutzer, J S

    1994-01-01

    A prospective study was conducted to evaluate pituitary-gonadal function and correlated parameters in 21 adult males with severe traumatic brain injury during acute inpatient rehabilitation. Serum concentrations of testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured within 1 week after the patient was transferred to the rehabilitation unit. Fourteen of 21 patients (67%) had abnormally low testosterone levels. One of 21 patients had a subnormal FSH level and one had a supranormal level. Three of 21 patients had subnormal LH levels and two had supranormal levels. There was no correlation between the severity of brain injury and the levels of testosterone, FSH or LH. The presence of increased intracranial pressure, hypoxia, skull fracture or abnormal CT findings had no significant influence on the levels of testosterone, FSH or LH. The high incidence of hypotestosteronaemia in survivors of severe traumatic brain injury is seemingly more related to accompanying physiological stressors rather than structural or neurochemical disruption of the hypothalamic-pituitary-gonadal axis. Early identification is important relative to the potential neuromedical and rehabilitative consequences of prolonged hypotestosteronaemia in this patient population.

  12. Experimental Models Combining Traumatic Brain Injury and Hypoxia.

    PubMed

    Thelin, Eric P

    2016-01-01

    Traumatic brain injury (TBI) is one of the most common causes of death and disability, and cerebral hypoxia is a frequently occurring harmful secondary event in TBI patients. The hypoxic conditions that occur on the scene of accident, where the airways are often obstructed or breathing is in other ways impaired, could be reproduced using animal TBI models where oxygen delivery is strictly controlled throughout the entire experimental procedure. Monitoring physiological parameters of the animal is of utmost importance in order to maintain an adequate quality of the experiment. Peripheral oxygen saturation, O2 pressure (pO2) in the blood, or fraction of inhaled O2 (FiO2) could be used as goals to validate the hypoxic conditions. Different models of traumatic brain injury could be used to inflict desired injury type, whereas effects then could be studied using radiological, physiological and functional tests. In order to confirm that the brain has been affected by a hypoxic injury, appropriate substances in the affected cerebral tissue, cerebrospinal fluid, or serum should be analyzed. PMID:27604734

  13. Predictors of Hypopituitarism in Patients with Traumatic Brain Injury.

    PubMed

    Silva, Paula P B; Bhatnagar, Saurabha; Herman, Seth D; Zafonte, Ross; Klibanski, Anne; Miller, Karen K; Tritos, Nicholas A

    2015-11-15

    Hypopituitarism may often occur in association with traumatic brain injury (TBI). Identification of reliable predictors of pituitary dysfunction is of importance in order to establish a rational testing approach. We searched the records of patients with TBI, who underwent neuroendocrine evaluation in our institution between 2007 and 2013. One hundred sixty-six adults (70% men) with TBI (median age: 41.6 years; range: 18-76) were evaluated at a median interval of 40.4 months (0.2-430.4).Of these, 31% had ≥1 pituitary deficiency, including 29% of patients with mild TBI and 35% with moderate/severe TBI. Growth hormone deficiency was the most common deficiency (21%); when body mass index (BMI)-dependent cutpoints were used, this was reduced to 15%. Central hypoadrenalism occurred in10%, who were more likely to have suffered a motor vehicle accident (MVA, p = 0.04), experienced post-traumatic seizures (p = 0.04), demonstrated any intracranial hemorrhage (p = 0.05), petechial brain hemorrhages (p = 0.017), or focal cortical parenchymal contusions (p = 0.02). Central hypothyroidism occurred in 8% and central hypogonadism in 12%; the latter subgroup had higher BMI (p = 0.03), were less likely to be working after TBI (p = 0.002), and had lower Global Assessment of Functioning (GAF) scores (p = 0.03). Central diabetes insipidus (DI) occurred in 6%, who were more likely to have experienced MVA (p < 0.001) or sustained moderate/severe TBI (p < 0.001). Patients with MVA and those with post-traumatic seizures, intracranial hemorrhage, petechial brain hemorrhages, and/or focal cortical contusions are at particular risk for serious pituitary dysfunction, including adrenal insufficiency and DI, and should be referred for neuroendocrine testing. However, a substantial proportion of patients without these risk factors also developed hypopituitarism. PMID:26413767

  14. Abstract representations of associated emotions in the human brain.

    PubMed

    Kim, Junsuk; Schultz, Johannes; Rohe, Tim; Wallraven, Christian; Lee, Seong-Whan; Bülthoff, Heinrich H

    2015-04-01

    Emotions can be aroused by various kinds of stimulus modalities. Recent neuroimaging studies indicate that several brain regions represent emotions at an abstract level, i.e., independently from the sensory cues from which they are perceived (e.g., face, body, or voice stimuli). If emotions are indeed represented at such an abstract level, then these abstract representations should also be activated by the memory of an emotional event. We tested this hypothesis by asking human participants to learn associations between emotional stimuli (videos of faces or bodies) and non-emotional stimuli (fractals). After successful learning, fMRI signals were recorded during the presentations of emotional stimuli and emotion-associated fractals. We tested whether emotions could be decoded from fMRI signals evoked by the fractal stimuli using a classifier trained on the responses to the emotional stimuli (and vice versa). This was implemented as a whole-brain searchlight, multivoxel activation pattern analysis, which revealed successful emotion decoding in four brain regions: posterior cingulate cortex (PCC), precuneus, MPFC, and angular gyrus. The same analysis run only on responses to emotional stimuli revealed clusters in PCC, precuneus, and MPFC. Multidimensional scaling analysis of the activation patterns revealed clear clustering of responses by emotion across stimulus types. Our results suggest that PCC, precuneus, and MPFC contain representations of emotions that can be evoked by stimuli that carry emotional information themselves or by stimuli that evoke memories of emotional stimuli, while angular gyrus is more likely to take part in emotional memory retrieval.

  15. Paediatric traumatic brain injury: a review of pertinent issues.

    PubMed

    Savage, Ronald C; DePompei, Roberta; Tyler, Janet; Lash, Marilyn

    2005-01-01

    Children with traumatic brain injury (TBI), regardless of the severity of the injury, often face challenges when living in home, school and community. Their needs are often overlooked and recognition of the long-term consequences is not always central to the management of the child in the school or community. This article provides references to pertinent literature and suggestions for intervention from the clinical experiences of four individuals with extensive experience of the family stresses, educational, cognitive-communicative and behavioural challenges that occur after TBI in children. It provides information regarding these issues, particularly educational situations, and suggests methods that may be useful for service providers and family members. PMID:16089249

  16. Alteration in synaptic junction proteins following traumatic brain injury.

    PubMed

    Merlo, Lucia; Cimino, Francesco; Angileri, Filippo Flavio; La Torre, Domenico; Conti, Alfredo; Cardali, Salvatore Massimiliano; Saija, Antonella; Germanò, Antonino

    2014-08-15

    Extensive research and scientific efforts have been focused on the elucidation of the pathobiology of cellular and axonal damage following traumatic brain injury (TBI). Conversely, few studies have specifically addressed the issue of synaptic dysfunction. Synaptic junction proteins may be involved in post-TBI alterations, leading to synaptic loss or disrupted plasticity. A Synapse Protein Database on synapse ontology identified 109 domains implicated in synaptic activities and over 5000 proteins, but few of these demonstrated to play a role in the synaptic dysfunction after TBI. These proteins are involved in neuroplasticity and neuromodulation and, most importantly, may be used as novel neuronal markers of TBI for specific intervention.

  17. Message retrieval for survivors of traumatic brain injury.

    PubMed

    Burke, Rebecca; Wassink, Kimberlee; Martin, Tracy; Seikel, Anthony J

    2008-03-01

    Survivors of traumatic brain injury often lose their ability to use natural speech to communicate and then rely on augmentative and alternative communication (AAC) devices. Survivors may also have concomitant cognitive communication disorders that negatively impact memory and organization skills. AAC devices need to incorporate a word retrieval organization strategy that is fast and effective. The current study compared the conditions of topic, place, and alphabet for message recognition. The participants were asked a delayed recall question to elicit a communicative response. Results showed that alphabet is significantly more accurate than place and significantly faster than place and topic. However, participants chose to retrieve words using all three strategies.

  18. Supporting the literacy skills of adolescents with traumatic brain injury.

    PubMed

    Krause, Miriam; Byom, Lindsey; Meulenbroek, Peter; Richards, Stephanie; O'Brien, Katy

    2015-02-01

    Traumatic brain injury (TBI) can affect developmental trajectories as well as language, attention, memory, executive functions, and other cognitive skills related to literacy. Literacy demands change through adolescence and into young adulthood, with academic literacy demands increasing and vocational literacy demands being introduced. Speech-language pathology services must evolve with the literacy needs of each client. This article discusses assessment and treatment approaches designed for adolescents with TBI and recommendations for adapting literacy interventions from the learning disabilities literature. Through proper assessment and intervention, speech-language pathologists can have a meaningful impact on the academic and vocational literacy needs of adolescents with TBI. PMID:25633145

  19. Traumatic Brain Injury and Behavior: A Practical Approach.

    PubMed

    McGee, Jeanie; Alekseeva, Nadejda; Chernyshev, Oleg; Minagar, Alireza

    2016-02-01

    Traumatic brain injury (TBI) is a complex neurologic and neuropathologic process that may affect the patient's behavior permanently. Clinically, TBI is associated with a wide gamut of neurologic and psychiatric disorders, such as amnesia, cognitive decline, seizures, attention and concentration deficits, depression, manic behavior, psychosis, hostile and violent behavior, and personality alterations. Therapy and rehabilitative efforts should be designed based on the type of injury and the patient's specific needs. Gaining familiarity with the behavioral disorders outlined in this article and understanding how to identify and treat them plays a significant role in the management of patients with TBI. PMID:26613995

  20. The neuroprotective effects of progesterone on traumatic brain injury: current status and future prospects

    PubMed Central

    Wei, Jing; Xiao, Guo-min

    2013-01-01

    Traumatic brain injury is the leading cause of morbidity and mortality in young adults. The secondary injury in traumatic brain injury consists of a complex cascade of processes that simultaneously react to the primary injury to the brain. This cascade has been the target of numerous therapeutic agents investigated over the last 30 years, but no neuroprotective treatment option is currently available that improve neurological outcome after traumatic brain injury. Progesterone has long been considered merely a female reproductive hormone. Numerous studies, however, show that progesterone has substantial pleiotropic properties as a neuroprotective agent in both animal models and humans. Here, we review the increasing evidence that progesterone can act as a neuroprotective agent to treat traumatic brain injury and the mechanisms underlying these effects. Additionally, we discuss the current progress of clinical studies on the application of progesterone in the treatment of traumatic brain injuries. PMID:24241345

  1. Neuroplasticity following non-penetrating traumatic brain injury.

    PubMed

    Levin, Harvey S

    2003-08-01

    The primary objective of this review is to examine the methodology and evidence for neuroplasticity operating in recovery from traumatic brain injury (TBI), as compared with previous findings in patients sustaining perinatal and infantile focal vascular lesions. The evidence to date indicates that the traditional view of enhanced reorganization of function after early focal brain lesions might apply to early focal brain lesions, but does not conform with studies of early severe diffuse brain injury. In contrast to early focal vascular lesions, young age confers no advantage in the outcome of severe diffuse brain injury. Disruption of myelination could potentially alter connectivity, a suggestion which could be confirmed through diffusion tensor imaging (DTI). Initial reports of DTI in TBI patients support the possibility that this technique can demonstrate alterations in white matter connections which are not seen on conventional magnetic resonance imaging (MRI) and might change over time or with interventions. Preliminary functional MRI studies of TBI patients indicate alterations in the pattern of brain activation, suggesting recruitment of more extensive cortical regions to perform tasks which stress computational resources. Functional MRI, coupled with DTI and possibly other imaging modalities holds the promise of elucidating mechanisms of neuroplasticity and repair following TBI. PMID:12850951

  2. Progressive inflammation-mediated neurodegeneration after traumatic brain or spinal cord injury.

    PubMed

    Faden, Alan I; Wu, Junfang; Stoica, Bogdan A; Loane, David J

    2016-02-01

    Traumatic brain injury (TBI) has been linked to dementia and chronic neurodegeneration. Described initially in boxers and currently recognized across high contact sports, the association between repeated concussion (mild TBI) and progressive neuropsychiatric abnormalities has recently received widespread attention, and has been termed chronic traumatic encephalopathy. Less well appreciated are cognitive changes associated with neurodegeneration in the brain after isolated spinal cord injury. Also under-recognized is the role of sustained neuroinflammation after brain or spinal cord trauma, even though this relationship has been known since the 1950s and is supported by more recent preclinical and clinical studies. These pathological mechanisms, manifested by extensive microglial and astroglial activation and appropriately termed chronic traumatic brain inflammation or chronic traumatic inflammatory encephalopathy, may be among the most important causes of post-traumatic neurodegeneration in terms of prevalence. Importantly, emerging experimental work demonstrates that persistent neuroinflammation can cause progressive neurodegeneration that may be treatable even weeks after traumatic injury.

  3. 78 FR 28546 - Secondary Service Connection for Diagnosable Illnesses Associated With Traumatic Brain Injury

    Federal Register 2010, 2011, 2012, 2013, 2014

    2013-05-15

    ... Traumatic Brain Injury Correction In proposed rule document 2012-29709 beginning on page 73366 in the issue...: Structural imaging of the brain. LOC--Loss of consciousness. AOC--Alteration of consciousness/mental...

  4. Traumatic Brain Injury: A Look at Alcohol and Other Drug Abuse Prevention.

    ERIC Educational Resources Information Center

    VSA Educational Services, Washington, DC. Resource Center on Substance Abuse Prevention and Disability.

    This leaflet examines alcohol and other drug abuse prevention for individuals with traumatic brain injury. The characteristics and incidence of traumatic brain injury (TBI) are noted. The implications of alcohol and other drug use are discussed, emphasizing that TBI is often related to lifestyles where alcohol and other drug abuse and risk taking…

  5. The Nature of Services Provided Students with Traumatic Brain Injury in Virginia.

    ERIC Educational Resources Information Center

    Virginia State Dept. of Education, Richmond.

    A survey of Virginia's local school divisions was conducted to obtain data on the number of students in Virginia with traumatic brain injury (TBI) and the nature of the services provided to them. A definition of traumatic brain injury is presented, and disorders resulting from TBI are listed, followed by a list of services required by this…

  6. Gait and Glasgow Coma Scale scores can predict functional recovery in patients with traumatic brain injury.

    PubMed

    Bilgin, Sevil; Guclu-Gunduz, Arzu; Oruckaptan, Hakan; Kose, Nezire; Celik, Bülent

    2012-09-01

    Fifty-one patients with mild (n = 14), moderate (n = 10) and severe traumatic brain injury (n = 27) received early rehabilitation. Level of consciousness was evaluated using the Glasgow Coma Score. Functional level was determined using the Glasgow Outcome Score, whilst mobility was evaluated using the Mobility Scale for Acute Stroke. Activities of daily living were assessed using the Barthel Index. Following Bobath neurodevelopmental therapy, the level of consciousness was significantly improved in patients with moderate and severe traumatic brain injury, but was not greatly influenced in patients with mild traumatic brain injury. Mobility and functional level were significantly improved in patients with mild, moderate and severe traumatic brain injury. Gait recovery was more obvious in patients with mild traumatic brain injury than in patients with moderate and severe traumatic brain injury. Activities of daily living showed an improvement but this was insignificant except for patients with severe traumatic brain injury. Nevertheless, complete recovery was not acquired at discharge. Multiple regression analysis showed that gait and Glasgow Coma Scale scores can be considered predictors of functional outcomes following traumatic brain injury. PMID:25624828

  7. Traumatic Brain Injury. Fact Sheet = Lesion Cerebral Traumatica (TBI). Hojas Informativas Sobre Discapacidades.

    ERIC Educational Resources Information Center

    National Information Center for Children and Youth with Disabilities, Washington, DC.

    This fact sheet, written in both English and Spanish, offers general information about traumatic brain injury. Information includes a definition, incidence, individual characteristics, and educational implications. The signs of traumatic brain injury are listed and include physical disabilities, difficulties with thinking, and social, behavioral,…

  8. Hydrogen-rich water attenuates brain damage and inflammation after traumatic brain injury in rats.

    PubMed

    Tian, Runfa; Hou, Zonggang; Hao, Shuyu; Wu, Weichuan; Mao, Xiang; Tao, Xiaogang; Lu, Te; Liu, Baiyun

    2016-04-15

    Inflammation and oxidative stress are the two major causes of apoptosis after traumatic brain injury (TBI). Most previous studies of the neuroprotective effects of hydrogen-rich water on TBI primarily focused on antioxidant effects. The present study investigated whether hydrogen-rich water (HRW) could attenuate brain damage and inflammation after traumatic brain injury in rats. A TBI model was induced using a controlled cortical impact injury. HRW or distilled water was injected intraperitoneally daily following surgery. We measured survival rate, brain edema, blood-brain barrier (BBB) breakdown and neurological dysfunction in all animals. Changes in inflammatory cytokines, inflammatory cells and Cho/Cr metabolites in brain tissues were also detected. Our results demonstrated that TBI-challenged rats exhibited significant brain injuries that were characterized by decreased survival rate and increased BBB permeability, brain edema, and neurological dysfunction, while HRW treatment ameliorated the consequences of TBI. HRW treatment also decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1β and HMGB1), inflammatory cell number (Iba1) and inflammatory metabolites (Cho) and increased the levels of an anti-inflammatory cytokine (IL-10) in the brain tissues of TBI-challenged rats. In conclusion, HRW could exert a neuroprotective effect against TBI and attenuate inflammation, which suggests HRW as an effective therapeutic strategy for TBI patients. PMID:26826009

  9. Blood-based diagnostics of traumatic brain injuries

    PubMed Central

    Mondello, Stefania; Muller, Uwe; Jeromin, Andreas; Streeter, Jackson; Hayes, Ronald L; Wang, Kevin KW

    2011-01-01

    Traumatic brain injury is a major health and socioeconomic problem that affects all societies. However, traditional approaches to the classification of clinical severity are the subject of debate and are being supplemented with structural and functional neuroimaging, as the need for biomarkers that reflect elements of the pathogenetic process is widely recognized. Basic science research and developments in the field of proteomics have greatly advanced our knowledge of the mechanisms involved in damage and have led to the discovery and rapid detection of new biomarkers that were not available previously. However, translating this research for patients' benefits remains a challenge. In this article, we summarize new developments, current knowledge and controversies, focusing on the potential role of these biomarkers as diagnostic, prognostic and monitoring tools of brain-injured patients. PMID:21171922

  10. Traumatic brain injury and NADPH oxidase: a deep relationship.

    PubMed

    Angeloni, Cristina; Prata, Cecilia; Dalla Sega, Francesco Vieceli; Piperno, Roberto; Hrelia, Silvana

    2015-01-01

    Traumatic brain injury (TBI) represents one of the major causes of mortality and disability in the world. TBI is characterized by primary damage resulting from the mechanical forces applied to the head as a direct result of the trauma and by the subsequent secondary injury due to a complex cascade of biochemical events that eventually lead to neuronal cell death. Oxidative stress plays a pivotal role in the genesis of the delayed harmful effects contributing to permanent damage. NADPH oxidases (Nox), ubiquitary membrane multisubunit enzymes whose unique function is the production of reactive oxygen species (ROS), have been shown to be a major source of ROS in the brain and to be involved in several neurological diseases. Emerging evidence demonstrates that Nox is upregulated after TBI, suggesting Nox critical role in the onset and development of this pathology. In this review, we summarize the current evidence about the role of Nox enzymes in the pathophysiology of TBI.

  11. Using anesthetics and analgesics in experimental traumatic brain injury.

    PubMed

    Rowe, Rachel K; Harrison, Jordan L; Thomas, Theresa C; Pauly, James R; Adelson, P David; Lifshitz, Jonathan

    2013-08-01

    Valid modeling of traumatic brain injury (TBI) requires accurate replication of both the mechanical forces that cause the primary injury and the conditions that lead to secondary injuries observed in human patients. The use of animals in TBI research is justified by the lack of in vitro or computer models that can sufficiently replicate the complex pathological processes involved. Measures to reduce nociception and distress must be implemented, but the administration of anesthetics and analgesics can influence TBI outcomes, threatening the validity of the research. In this review, the authors present evidence for the interference of anesthetics and analgesics in the natural course of brain injury in animal models of TBI. They suggest that drugs should be selected for or excluded from experimental TBI protocols on the basis of IACUC-approved experimental objectives in order to protect animal welfare and preserve the validity of TBI models. PMID:23877609

  12. Impulsive Pressurization of Neuronal Cells for Traumatic Brain Injury Study

    PubMed Central

    Feng, Ruqiang; Lim, Jung Yul

    2011-01-01

    A novel impulsive cell pressurization experiment has been developed using a Kolsky bar device to investigate blast-induced traumatic brain injury (TBI). We demonstrate in this video article how blast TBI-relevant impulsive pressurization is applied to the neuronal cells in vitro. This is achieved by using well-controlled pressure pulse created by a specialized Kolsky bar device, with complete pressure history within the cell pressurization chamber recorded. Pressurized neuronal cells are inspected immediately after pressurization, or further incubated to examine the long-term effects of impulsive pressurization on neurite/axonal outgrowth, neuronal gene expression, apoptosis, etc. We observed that impulsive pressurization at about 2 MPa induces distinct neurite loss relative to unpressurized cells. Our technique provides a novel method to investigate the molecular/cellular mechanisms of blast TBI, via impulsive pressurization of brain cells at well-controlled pressure magnitude and duration. PMID:22005926

  13. Traumatic Brain Injury and NADPH Oxidase: A Deep Relationship

    PubMed Central

    Prata, Cecilia; Vieceli Dalla Sega, Francesco; Piperno, Roberto; Hrelia, Silvana

    2015-01-01

    Traumatic brain injury (TBI) represents one of the major causes of mortality and disability in the world. TBI is characterized by primary damage resulting from the mechanical forces applied to the head as a direct result of the trauma and by the subsequent secondary injury due to a complex cascade of biochemical events that eventually lead to neuronal cell death. Oxidative stress plays a pivotal role in the genesis of the delayed harmful effects contributing to permanent damage. NADPH oxidases (Nox), ubiquitary membrane multisubunit enzymes whose unique function is the production of reactive oxygen species (ROS), have been shown to be a major source of ROS in the brain and to be involved in several neurological diseases. Emerging evidence demonstrates that Nox is upregulated after TBI, suggesting Nox critical role in the onset and development of this pathology. In this review, we summarize the current evidence about the role of Nox enzymes in the pathophysiology of TBI. PMID:25918580

  14. Neuroimaging biomarkers in mild traumatic brain injury (mTBI).

    PubMed

    Bigler, Erin D

    2013-09-01

    Reviewed herein are contemporary neuroimaging methods that detect abnormalities associated with mild traumatic brain injury (mTBI). Despite advances in demonstrating underlying neuropathology in a subset of individuals who sustain mTBI, considerable disagreement persists in neuropsychology about mTBI outcome and metrics for evaluation. This review outlines a thesis for the select use of sensitive neuroimaging methods as potential biomarkers of brain injury recognizing that the majority of individuals who sustain an mTBI recover without neuroimaging signs or neuropsychological sequelae detected with methods currently applied. Magnetic resonance imaging (MRI) provides several measures that could serve as mTBI biomarkers including the detection of hemosiderin and white matter abnormalities, assessment of white matter integrity derived from diffusion tensor imaging (DTI), and quantitative measures that directly assess neuroanatomy. Improved prediction of neuropsychological outcomes in mTBI may be achieved with the use of targeted neuroimaging markers.

  15. Brain activity accompanying perception of implied motion in abstract paintings.

    PubMed

    Kim, Chai-Youn; Blake, Randolph

    2007-01-01

    Early 20th century artists including Duchamp and Balla tried to portray moving objects on a static canvas by superimposing objects in successive portrayals of an action. We investigated whether implied motion in those paintings is associated with activation of motion-sensitive area MT+. In Experiment 1, we found that observers rated these kinds of paintings higher in portraying motion than they did other abstract paintings in which motion is not intended. We also found that observers who had previously experienced abstract paintings with implied motion tended to give higher motion ratings to that class of paintings. In Experiment 2, we used functional magnetic resonance imaging (fMRI) to measure brain activity of observers while viewing abstract paintings receiving the highest and the lowest motion rating scores in Experiment 1. We found MT+, but not primary visual cortex (V1), showed greater BOLD responses to abstract paintings with implied motion than to abstract paintings with little motion impression, but only in observers with prior experience viewing those kinds of paintings. These results imply that the neural machinery ordinarily engaged during perception of real visual motion is activated when people view paintings explicitly designed to convey a sense of visual motion. Experience, however, is necessary to achieve this sense of motion.

  16. Progesterone for Neuroprotection in Pediatric Traumatic Brain Injury

    PubMed Central

    Robertson, Courtney L.; Fidan, Emin; Stanley, Rachel M.; MHSA; Noje, Corina; Bayir, Hülya

    2016-01-01

    Objective To provide an overview of the preclinical literature on progesterone for neuroprotection after traumatic brain injury (TBI), and to describe unique features of developmental brain injury that should be considered when evaluating the therapeutic potential for progesterone treatment after pediatric TBI. Data Sources National Library of Medicine PubMed literature review. Data Selection The mechanisms of neuroprotection by progesterone are reviewed, and the preclinical literature using progesterone treatment in adult animal models of TBI are summarized. Unique features of the developing brain that could either enhance or limit the efficacy of neuroprotection by progesterone are discussed, and the limited preclinical literature using progesterone after acute injury to the developing brain is described. Finally, the current status of clinical trials of progesterone for adult TBI is reviewed. Data Extraction and Synthesis Progesterone is a pleotropic agent with beneficial effects on secondary injury cascades that occur after TBI, including cerebral edema, neuroinflammation, oxidative stress, and excitotoxicity. More than 40 studies have used progesterone for treatment after TBI in adult animal models, with results summarized in tabular form. However, very few studies have evaluated progesterone in pediatric animal models of brain injury. To date, two human Phase II trials of progesterone for adult TBI have been published, and two multi-center Phase III trials are underway. Conclusions The unique features of the developing brain from that of a mature adult brain make it necessary to independently study progesterone in clinically relevant, immature animal models of TBI. Additional preclinical studies could lead to the development of a novel neuroprotective therapy that could reduce the long-term disability in head-injured children, and could potentially provide benefit in other forms of pediatric brain injury (global ischemia, stroke, statue epilepticus). PMID

  17. Mild Traumatic Brain Injury Update: Forensic Neuropsychiatric Implications.

    PubMed

    Wortzel, Hal S; Granacher, Robert P

    2015-12-01

    Traumatic brain injury (TBI) involves a wide range of potential neuropsychiatric outcomes, from death or profound impairment to full and fast recovery. This circumstance has contributed to an atmosphere with considerable potential for both clinical confusion and unjustified medicolegal outcomes. Given that mild (m)TBI accounts for most (∼80%) TBI events and is generally associated with an excellent prognosis, the risk for erroneous clinical formulations and unmerited legal outcomes seems particularly high in cases involving mTBI. In this article, we summarize the recent results published by the International Collaboration on Mild Traumatic Brain Injury Prognosis (ICMTBIP) and the new approach of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, to TBI, and we explore the clinical and medicolegal implications. Symptoms that emerge after mTBI remain nonspecific, and potential etiologies are diverse. Clinicians and medicolegal experts should be familiar with the natural history of mTBI, able to recognize atypical outcomes, and willing to search for alternative explanations when confronted with persistent or severe impairment.

  18. Altered oscillatory brain dynamics after repeated traumatic stress

    PubMed Central

    Kolassa, Iris-Tatjana; Wienbruch, Christian; Neuner, Frank; Schauer, Maggie; Ruf, Martina; Odenwald, Michael; Elbert, Thomas

    2007-01-01

    Background Repeated traumatic experiences, e.g. torture and war, lead to functional and structural cerebral changes, which should be detectable in cortical dynamics. Abnormal slow waves produced within circumscribed brain regions during a resting state have been associated with lesioned neural circuitry in neurological disorders and more recently also in mental illness. Methods Using magnetoencephalographic (MEG-based) source imaging, we mapped abnormal distributions of generators of slow waves in 97 survivors of torture and war with posttraumatic stress disorder (PTSD) in comparison to 97 controls. Results PTSD patients showed elevated production of focally generated slow waves (1–4 Hz), particularly in left temporal brain regions, with peak activities in the region of the insula. Furthermore, differential slow wave activity in right frontal areas was found in PTSD patients compared to controls. Conclusion The insula, as a site of multimodal convergence, could play a key role in understanding the pathophysiology of PTSD, possibly accounting for what has been called posttraumatic alexithymia, i.e., reduced ability to identify, express and regulate emotional responses to reminders of traumatic events. Differences in activity in right frontal areas may indicate a dysfunctional PFC, which may lead to diminished extinction of conditioned fear and reduced inhibition of the amygdala. PMID:17941996

  19. Voluntary Exercise Preconditioning Activates Multiple Antiapoptotic Mechanisms and Improves Neurological Recovery after Experimental Traumatic Brain Injury

    PubMed Central

    Zhao, Zaorui; Sabirzhanov, Boris; Wu, Junfang; Faden, Alan I.

    2015-01-01

    Abstract Physical activity can attenuate neuronal loss, reduce neuroinflammation, and facilitate recovery after brain injury. However, little is known about the mechanisms of exercise-induced neuroprotection after traumatic brain injury (TBI) or its modulation of post-traumatic neuronal cell death. Voluntary exercise, using a running wheel, was conducted for 4 weeks immediately preceding (preconditioning) moderate-level controlled cortical impact (CCI), a well-established experimental TBI model in mice. Compared to nonexercised controls, exercise preconditioning (pre-exercise) improved recovery of sensorimotor performance in the beam walk task, as well as cognitive/affective functions in the Morris water maze, novel object recognition, and tail-suspension tests. Further, pre-exercise reduced lesion size, attenuated neuronal loss in the hippocampus, cortex, and thalamus, and decreased microglial activation in the cortex. In addition, exercise preconditioning activated the brain-derived neurotrophic factor pathway before trauma and amplified the injury-dependent increase in heat shock protein 70 expression, thus attenuating key apoptotic pathways. The latter include reduction in CCI-induced up-regulation of proapoptotic B-cell lymphoma 2 (Bcl-2)-homology 3–only Bcl-2 family molecules (Bid, Puma), decreased mitochondria permeabilization with attenuated release of cytochrome c and apoptosis-inducing factor (AIF), reduced AIF translocation to the nucleus, and attenuated caspase activation. Given these neuroprotective actions, voluntary physical exercise may serve to limit the consequences of TBI. PMID:25419789

  20. The Presence and Role of Iron in Mild Traumatic Brain Injury: An Imaging Perspective

    PubMed Central

    Nisenbaum, Eric J.; Novikov, Dmitry S.

    2014-01-01

    Abstract Mild traumatic brain injury (mTBI), although often presenting without the gross structural abnormalities seen in more severe forms of brain trauma, can nonetheless result in lingering cognitive and behavioral problems along with subtle alterations in brain structure and function. Repeated injuries are associated with brain atrophy and dementia in the form of chronic traumatic encephalopathy (CTE). The mechanisms underlying these dysfunctions are poorly understood. There is a growing body of evidence that brain iron is abnormal after TBI, and brain iron has also been implicated in a host of neurodegenerative disorders. The purpose of this article is to review evidence about the function of iron in the pathophysiology of mTBI and the role that advanced imaging modalities can play in further elucidating said function. MRI techniques sensitive to field inhomogeneities provide supporting evidence for both deep gray matter non-heme iron accumulation as well as focal microhemorrhage resulting from mTBI. In addition, there is evidence that iron may contribute to pathology after mTBI through a number of mechanisms, including generation of reactive oxygen species (ROS), exacerbation of oxidative stress from other sources, and encouragement of tau phosphorylation and the formation of neurofibrillary tangles. Finally, recent animal studies suggest that iron may serve as a therapeutic target in mitigating the effects of mTBI. However, research on the presence and role of iron in mTBI and CTE is still relatively sparse, and further work is necessary to elucidate issues such as the sources of increased iron and the chain of secondary injury. PMID:24295521

  1. Magnetic micelles for DNA delivery to rat brains after mild traumatic brain injury.

    PubMed

    Das, Mahasweta; Wang, Chunyan; Bedi, Raminder; Mohapatra, Shyam S; Mohapatra, Subhra

    2014-10-01

    Traumatic brain injury (TBI) causes significant mortality, long term disability and psychological symptoms. Gene therapy is a promising approach for treatment of different pathological conditions. Here we tested chitosan and polyethyleneimine (PEI)-coated magnetic micelles (CP-mag micelles or CPMMs), a potential MRI contrast agent, to deliver a reporter DNA to the brain after mild TBI (mTBI). CPMM-tomato plasmid (ptd) conjugate expressing a red-fluorescent protein (RFP) was administered intranasally immediately after mTBI or sham surgery in male SD rats. Evans blue extravasation following mTBI suggested CPMM-ptd entry into the brain via the compromised blood-brain barrier. Magnetofection increased the concentration of CPMMs in the brain. RFP expression was observed in the brain (cortex and hippocampus), lung and liver 48 h after mTBI. CPMM did not evoke any inflammatory response by themselves and were excreted from the body. These results indicate the possibility of using intranasally administered CPMM as a theranostic vehicle for mTBI. From the clinical editor: In this study, chitosan and PEI-coated magnetic micelles (CPMM) were demonstrated as potentially useful vehicles in traumatic brain injury in a rodent model. Magnetofection increased the concentration of CPMMs in the brain and, after intranasal delivery, CPMM did not evoke any inflammatory response and were excreted from the body. PMID:24486465

  2. Characterization of Pressure Distribution in Penetrating Traumatic Brain Injuries

    PubMed Central

    Davidsson, Johan; Risling, Mårten

    2015-01-01

    Severe impacts to the head commonly lead to localized brain damage. Such impacts may also give rise to temporary pressure changes that produce secondary injuries in brain volumes distal to the impact site. Monitoring pressure changes in a clinical setting is difficult; detailed studies into the effect of pressure changes in the brain call for the development and use of animal models. The aim of this study is to characterize the pressure distribution in an animal model of penetrating traumatic brain injuries (pTBI). This data may be used to validate mathematical models of the animal model and to facilitate correlation studies between pressure changes and pathology. Pressure changes were measured in rat brains while subjected to pTBI for a variety of different probe velocities and shapes; pointy, blunt, and flat. Experiments on ballistic gel samples were carried out to study the formation of any temporary cavities. In addition, pressure recordings from the gel experiments were compared to values recorded in the animal experiments. The pTBI generated short lasting pressure changes in the brain tissue; the pressure in the contralateral ventricle (CLV) increased to 8 bar followed by a drop to 0.4 bar when applying flat probes. The pressure changes in the periphery of the probe, in the Cisterna Magna, and the spinal canal, were significantly less than those recorded in the CLV or the vicinity of the skull base. High-speed videos of the gel samples revealed the formation of spherically shaped cavities when flat and spherical probes were applied. Pressure changes in the gel were similar to those recorded in the animals, although amplitudes were lower in the gel samples. We concluded cavity expansion rate rather than cavity size correlated with pressure changes in the gel or brain secondary to probe impact. The new data can serve as validation data for finite element models of the trauma model and the animal and to correlate physical measurements with secondary injuries

  3. Lactate: Brain Fuel in Human Traumatic Brain Injury: A Comparison with Normal Healthy Control Subjects

    PubMed Central

    Martin, Neil A.; Horning, Michael A.; McArthur, David L.; Hovda, David A.; Vespa, Paul; Brooks, George A.

    2015-01-01

    Abstract We evaluated the hypothesis that lactate shuttling helps support the nutritive needs of injured brains. To that end, we utilized dual isotope tracer [6,6-2H2]glucose, that is, D2-glucose, and [3-13C]lactate techniques involving arm vein tracer infusion along with simultaneous cerebral (arterial [art] and jugular bulb [JB]) blood sampling. Traumatic brain injury (TBI) patients with nonpenetrating brain injuries (n=12) were entered into the study following consent of patients' legal representatives. Written and informed consent was obtained from control volunteers (n=6). Patients were studied 5.7±2.2 (mean±SD) days post-injury; during periods when arterial glucose concentration tended to be higher in TBI patients. As in previous investigations, the cerebral metabolic rate for glucose (CMRgluc, i.e., net glucose uptake) was significantly suppressed following TBI (p<0.001). However, lactate fractional extraction, an index of cerebral lactate uptake related to systemic lactate supply, approximated 11% in both healthy control subjects and TBI patients. Further, neither the CMR for lactate (CMRlac, i.e., net lactate release), nor the tracer-measured cerebral lactate uptake differed between healthy controls and TBI patients. The percentages of lactate tracer taken up and released as 13CO2 into the JB accounted for 92% and 91% for control and TBI conditions, respectively, suggesting that most cerebral lactate uptake was oxidized following TBI. Comparisons of isotopic enrichments of lactate oxidation from infused [3-13C]lactate tracer and 13C-glucose produced during hepatic and renal gluconeogenesis (GNG) showed that 75–80% of 13CO2 released into the JB was from lactate and that the remainder was from the oxidation of glucose secondarily labeled from lactate. Hence, either directly as lactate uptake, or indirectly via GNG, peripheral lactate production accounted for ∼70% of carbohydrate (direct lactate uptake+uptake of glucose from lactate) consumed by the

  4. Abstract representations of associated emotions in the human brain.

    PubMed

    Kim, Junsuk; Schultz, Johannes; Rohe, Tim; Wallraven, Christian; Lee, Seong-Whan; Bülthoff, Heinrich H

    2015-04-01

    Emotions can be aroused by various kinds of stimulus modalities. Recent neuroimaging studies indicate that several brain regions represent emotions at an abstract level, i.e., independently from the sensory cues from which they are perceived (e.g., face, body, or voice stimuli). If emotions are indeed represented at such an abstract level, then these abstract representations should also be activated by the memory of an emotional event. We tested this hypothesis by asking human participants to learn associations between emotional stimuli (videos of faces or bodies) and non-emotional stimuli (fractals). After successful learning, fMRI signals were recorded during the presentations of emotional stimuli and emotion-associated fractals. We tested whether emotions could be decoded from fMRI signals evoked by the fractal stimuli using a classifier trained on the responses to the emotional stimuli (and vice versa). This was implemented as a whole-brain searchlight, multivoxel activation pattern analysis, which revealed successful emotion decoding in four brain regions: posterior cingulate cortex (PCC), precuneus, MPFC, and angular gyrus. The same analysis run only on responses to emotional stimuli revealed clusters in PCC, precuneus, and MPFC. Multidimensional scaling analysis of the activation patterns revealed clear clustering of responses by emotion across stimulus types. Our results suggest that PCC, precuneus, and MPFC contain representations of emotions that can be evoked by stimuli that carry emotional information themselves or by stimuli that evoke memories of emotional stimuli, while angular gyrus is more likely to take part in emotional memory retrieval. PMID:25855179

  5. The Evolution of Post-Traumatic Stress Disorder following Moderate-to-Severe Traumatic Brain Injury.

    PubMed

    Alway, Yvette; Gould, Kate Rachel; McKay, Adam; Johnston, Lisa; Ponsford, Jennie

    2016-05-01

    Increasing evidence indicates that post-traumatic stress disorder (PTSD) may develop following traumatic brain injury (TBI), despite most patients having no conscious memory of their accident. This prospective study examined the frequency, timing of onset, symptom profile, and trajectory of PTSD and its psychiatric comorbidities during the first 4 years following moderate-to-severe TBI. Participants were 85 individuals (78.8% male) with moderate or severe TBI recruited following admission to acute rehabilitation between 2005 and 2010. Using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Disorders (SCID-I), participants were evaluated for pre- and post-injury PTSD soon after injury and reassessed at 6 months, 12 months, 2 years, 3 years, and 4 years post-injury. Over the first 4 years post-injury, 17.6% developed injury-related PTSD, none of whom had PTSD prior to injury. PTSD onset peaked between 6 and 12 months post-injury. The majority of PTSD cases (66.7%) had a delayed-onset, which for a third was preceded by subsyndromal symptoms in the first 6 months post-injury. PTSD frequency increased over the first year post-injury, remained stable during the second year, and gradually declined thereafter. The majority of subjects with PTSD experienced a chronic symptom course and all developed one or more than one comorbid psychiatric disorder, with mood, other anxiety, and substance-use disorders being the most common. Despite event-related amnesia, post-traumatic stress symptoms, including vivid re-experiencing phenomena, may develop following moderate-to-severe TBI. Onset is typically delayed and symptoms may persist for several years post-injury.

  6. Traumatic Brain Injury and the Effect on the Brain-Gut Axis.

    PubMed

    Kharrazian, Datis

    2015-08-01

    Traumatic brain injury (TBI) is a leading cause of disability worldwide. One commonly overlooked effect of TBI is the disruption of the brain-gut axis, leading to gastrointestinal dysfunction. The brain-gut axis consists of the cortical areas of the insular cortex, cingulate, and hypothalamus that have bidirectional communication with the visceral enteric nervous system through afferent and efferent projections into the pontine vagal complex and nucleus tractus solitarius. Communication with the brain also occurs through messenger signals from the gut's microbiota, involving gut peptides, cytokines, and lipopolysaccharides. Disruption of the brain-gut axis from TBI can lead to a chronic, inflammatory, vicious sequela, involving both the brain and the gastrointestinal system, with both neuroregulatory and neuroimmunological loops. PMID:26348611

  7. Postnatal Neural Stem Cells in Treating Traumatic Brain Injury.

    PubMed

    Gazalah, Hussein; Mantash, Sarah; Ramadan, Naify; Al Lafi, Sawsan; El Sitt, Sally; Darwish, Hala; Azari, Hassan; Fawaz, Lama; Ghanem, Noël; Zibara, Kazem; Boustany, Rose-Mary; Kobeissy, Firas; Soueid, Jihane

    2016-01-01

    Traumatic brain injury (TBI) is one of the leading causes of death and disabilities worldwide. It affects approximately 1.5 million people each year and is associated with severe post-TBI symptoms such as sensory and motor deficits. Several neuro-therapeutic approaches ranging from cell therapy interventions such as the use of neural stem cells (NSCs) to drug-based therapies have been proposed for TBI management. Successful cell-based therapies are tightly dependent on reproducible preclinical animal models to ensure safety and optimal therapeutic benefits. In this chapter, we describe the isolation of NSCs from neonatal mouse brain using the neurosphere assay in culture. Subsequently, dissociated neurosphere-derived cells are used for transplantation into the ipsilateral cortex of a controlled cortical impact (CCI) TBI model in C57BL/6 mice. Following intra-cardiac perfusion and brain removal, the success of NSC transplantation is then evaluated using immunofluorescence in order to assess neurogenesis along with gliosis in the ipsilateral coronal brain sections. Behavioral tests including rotarod and pole climbing are conducted to evaluate the motor activity post-treatment intervention. PMID:27604746

  8. Mild traumatic brain injury and neural recovery: rethinking the debate.

    PubMed

    Ruff, Ronald M

    2011-01-01

    A debate exists concerning whether a mild traumatic brain injury (MTBI) can cause permanent brain-based residuals. This debate is examined by reviewing meta-analytic studies that found no significant effect sizes between large samples of patients with and without MTBI at three months post-accident. In contrast, research studies with MTBI patients have captured cognitive deficits corroborated by positive neuroimaging, which supports the viewpoint that brain-based postconcussive disorders likely exist in a small minority of individuals. Ongoing hurdles that likely contribute to this debate are identified. This includes the lack of agreed upon definitions; substantial differences exist between the ICD-10 definition for Postconcussion Syndrome and the DSM-IV-TR definition for Postconcussional Disorder. Confining the debate to brain-based versus psychologically-based viewpoints results in a false dichotomy. Instead, a more refined sub-classification of the postconcussive complex is proposed that captures different constellations across the physical, emotional, and cognitive symptoms complex. Moreover, this diagnostic framework attempts to expand discipline-based approaches with a patient-based understanding. PMID:21558623

  9. Decompressive surgery in the treatment of traumatic brain injury.

    PubMed

    Piek, Jürgen

    2002-04-01

    According to European Brain Injury Consortium (EBIC) and American Brain Injury Consortium (ABIC) guidelines for severe head injuries, decompressive craniectomy is one therapeutic option for brain edema that does not respond to conventional therapeutic measures. As a result of the failure of all recently developed drugs to improve outcome in this patient group, decompressive craniectomy has experienced a revival during the last decade. Although class I studies of this subject are still lacking, there is strong evidence from prospective, uncontrolled trials that such an operation improves outcome in general and also has beneficial effects on various physiologic parameters that are known to be independent predictors for poor outcome. Whether this operation should be performed in a protocol-driven or in a prophylactic manner remains unclear. Decompressive craniectomy may, however, be the only method available in developing countries with limited ICU and monitoring resources. Prospectively controlled and randomized studies to definitively evaluate the effect of this old neurosurgical method on outcome in patients with traumatic brain injury (TBI) are forthcoming.

  10. Investigation of blast-induced traumatic brain injury

    PubMed Central

    Ludwigsen, John S.; Ford, Corey C.

    2014-01-01

    Objective Many troops deployed in Iraq and Afghanistan have sustained blast-related, closed-head injuries from being within non-lethal distance of detonated explosive devices. Little is known, however, about the mechanisms associated with blast exposure that give rise to traumatic brain injury (TBI). This study attempts to identify the precise conditions of focused stress wave energy within the brain, resulting from blast exposure, which will correlate with a threshold for persistent brain injury. Methods This study developed and validated a set of modelling tools to simulate blast loading to the human head. Using these tools, the blast-induced, early-time intracranial wave motions that lead to focal brain damage were simulated. Results The simulations predict the deposition of three distinct wave energy components, two of which can be related to injury-inducing mechanisms, namely cavitation and shear. Furthermore, the results suggest that the spatial distributions of these damaging energy components are independent of blast direction. Conclusions The predictions reported herein will simplify efforts to correlate simulation predictions with clinical measures of TBI and aid in the development of protective headwear. PMID:24766453

  11. Functional neuroimaging of traumatic brain injury: advances and clinical utility

    PubMed Central

    Irimia, Andrei; Van Horn, John Darrell

    2015-01-01

    Functional deficits due to traumatic brain injury (TBI) can have significant and enduring consequences upon patients’ life quality and expectancy. Although functional neuroimaging is essential for understanding TBI pathophysiology, an insufficient amount of effort has been dedicated to the task of translating functional neuroimaging findings into information with clinical utility. The purpose of this review is to summarize the use of functional neuroimaging techniques – especially functional magnetic resonance imaging, diffusion tensor imaging, positron emission tomography, magnetic resonance spectroscopy, and electroencephalography – for advancing current knowledge of TBI-related brain dysfunction and for improving the rehabilitation of TBI patients. We focus on seven core areas of functional deficits, namely consciousness, motor function, attention, memory, higher cognition, personality, and affect, and, for each of these, we summarize recent findings from neuroimaging studies which have provided substantial insight into brain function changes due to TBI. Recommendations are also provided to aid in setting the direction of future neuroimaging research and for understanding brain function changes after TBI. PMID:26396520

  12. Social dysfunction after pediatric traumatic brain injury: A translational perspective.

    PubMed

    Ryan, Nicholas P; Catroppa, Cathy; Godfrey, Celia; Noble-Haeusslein, Linda J; Shultz, Sandy R; O'Brien, Terence J; Anderson, Vicki; Semple, Bridgette D

    2016-05-01

    Social dysfunction is common after traumatic brain injury (TBI), contributing to reduced quality of life for survivors. Factors which influence the development or persistence of social deficits after injury remain poorly understood, particularly in the context of ongoing brain maturation during childhood and adolescence. Aberrant social interactions have recently been modeled in adult and juvenile rodents after experimental TBI, providing an opportunity to gain new insights into the underlying neurobiology of these behaviors. Here, we review our current understanding of social dysfunction in both humans and rodent models of TBI, with a focus on brain injuries acquired during early development. Modulators of social outcomes are discussed, including injury-related and environmental risk and resilience factors. Disruption of social brain network connectivity and aberrant neuroendocrine function are identified as potential mechanisms of social impairments after pediatric TBI. Throughout, we highlight the overlap and disparities between outcome measures and findings from clinical and experimental approaches, and explore the translational potential of future research to prevent or ameliorate social dysfunction after childhood TBI. PMID:26949224

  13. Decoding Hippocampal Signaling Deficits after Traumatic Brain Injury

    PubMed Central

    Atkins, Coleen M.

    2012-01-01

    There are more than 3.17 million people coping with long-term disabilities due to traumatic brain injury (TBI) in the United States. The majority of TBI research is focused on developing acute neuroprotective treatments to prevent or minimize these long-term disabilities. Therefore, chronic TBI survivors represent a large, underserved population that could significantly benefit from a therapy that capitalizes on the endogenous recovery mechanisms occurring during the weeks to months following brain trauma. Previous studies have found that the hippocampus is highly vulnerable to brain injury, in both experimental models of TBI and during human TBI. Although often not directly mechanically injured by the head injury, in the weeks to months following TBI, the hippocampus undergoes atrophy and exhibits deficits in long-term potentiation (LTP), a persistent increase in synaptic strength that is considered to be a model of learning and memory. Decoding the chronic hippocampal LTP and cell signaling deficits after brain trauma will provide new insights into the molecular mechanisms of hippocampal-dependent learning impairments caused by TBI and facilitate the development of effective therapeutic strategies to improve hippocampal-dependent learning for chronic survivors of TBI. PMID:23227133

  14. Low level laser therapy for traumatic brain injury

    NASA Astrophysics Data System (ADS)

    Wu, Qiuhe; Huang, Ying-Ying; Dhital, Saphala; Sharma, Sulbha K.; Chen, Aaron C.-H.; Whalen, Michael J.; Hamblin, Michael R.

    2010-02-01

    Low level laser (or light) therapy (LLLT) has been clinically applied for many indications in medicine that require the following processes: protection from cell and tissue death, stimulation of healing and repair of injuries, and reduction of pain, swelling and inflammation. One area that is attracting growing interest is the use of transcranial LLLT to treat stroke and traumatic brain injury (TBI). The fact that near-infrared light can penetrate into the brain would allow non-invasive treatment to be carried out with a low likelihood of treatment-related adverse events. LLLT may have beneficial effects in the acute treatment of brain damage injury by increasing respiration in the mitochondria, causing activation of transcription factors, reducing key inflammatory mediators, and inhibiting apoptosis. We tested LLLT in a mouse model of TBI produced by a controlled weight drop onto the skull. Mice received a single treatment with 660-nm, 810-nm or 980-nm laser (36 J/cm2) four hours post-injury and were followed up by neurological performance testing for 4 weeks. Mice with moderate to severe TBI treated with 660- nm and 810-nm laser had a significant improvement in neurological score over the course of the follow-up and histological examination of the brains at sacrifice revealed less lesion area compared to untreated controls. Further studies are underway.

  15. Traumatic brain injury in mice and pentadecapeptide BPC 157 effect.

    PubMed

    Tudor, Mario; Jandric, Ivan; Marovic, Anton; Gjurasin, Miroslav; Perovic, Darko; Radic, Bozo; Blagaic, Alenka Boban; Kolenc, Danijela; Brcic, Luka; Zarkovic, Kamelija; Seiwerth, Sven; Sikiric, Predrag

    2010-02-25

    Gastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, an anti-ulcer peptide, efficient in inflammatory bowel disease trials (PL 14736), no toxicity reported, improved muscle crush injury. After an induced traumatic brain injury (TBI) in mice by a falling weight, BPC 157 regimens (10.0microg, 10.0ng/kgi.p.) demonstrated a marked attenuation of damage with an improved early outcome and a minimal postponed mortality throughout a 24h post-injury period. Ultimately, the traumatic lesions (subarachnoidal and intraventricular haemorrhage, brain laceration, haemorrhagic laceration) were less intense and consecutive brain edema had considerably improved. Given prophylactically (30 min before TBI) the improved conscious/unconscious/death ratio in TBI-mice was after force impulses of 0.068 Ns, 0.093 Ns, 0.113 Ns, 0.130 Ns, 0.145 Ns, and 0.159 Ns. Counteraction (with a reduction of unconsciousness, lower mortality) with both microg- and ng-regimens included the force impulses of 0.068-0.145 Ns. A higher regimen presented effectiveness also against the maximal force impulse (0.159 Ns). Furthermore, BPC 157 application immediately prior to injury was beneficial in mice subjected to force impulses of 0.093 Ns-TBI. For a more severe force impulse (0.130 Ns, 0.145 Ns, or 0159 Ns), the time-relation to improve the conscious/unconscious/death ratio was: 5 min (0.130 Ns-TBI), 20 min (0.145 Ns-TBI) or 30 min (0.159 Ns-TBI). PMID:19931318

  16. Impaired response inhibition in veterans with post-traumatic stress disorder and mild traumatic brain injury.

    PubMed

    Swick, Diane; Honzel, Nikki; Larsen, Jary; Ashley, Victoria; Justus, Timothy

    2012-09-01

    Combat veterans with post-traumatic stress disorder (PTSD) can show impairments in executive control and increases in impulsivity. The current study examined the effects of PTSD on motor response inhibition, a key cognitive control function. A Go/NoGo task was administered to veterans with a diagnosis of PTSD based on semi-structured clinical interview using DSM-IV criteria (n = 40) and age-matched control veterans (n = 33). Participants also completed questionnaires to assess self-reported levels of PTSD and depressive symptoms. Performance measures from the patients (error rates and reaction times) were compared to those from controls. PTSD patients showed a significant deficit in response inhibition, committing more errors on NoGo trials than controls. Higher levels of PTSD and depressive symptoms were associated with higher error rates. Of the three symptom clusters, re-experiencing was the strongest predictor of performance. Because the co-morbidity of mild traumatic brain injury (mTBI) and PTSD was high in this population, secondary analyses compared veterans with PTSD+mTBI (n = 30) to veterans with PTSD only (n = 10). Although preliminary, results indicated the two patient groups did not differ on any measure (p > .88). Since cognitive impairments could hinder the effectiveness of standard PTSD therapies, incorporating treatments that strengthen executive functions might be considered in the future. (JINS, 2012, 18, 1-10).

  17. Levetiracetam Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy.

    PubMed

    Browning, Megan; Shear, Deborah A; Bramlett, Helen M; Dixon, C Edward; Mondello, Stefania; Schmid, Kara E; Poloyac, Samuel M; Dietrich, W Dalton; Hayes, Ronald L; Wang, Kevin K W; Povlishock, John T; Tortella, Frank C; Kochanek, Patrick M

    2016-03-15

    Levetiracetam (LEV) is an antiepileptic agent targeting novel pathways. Coupled with a favorable safety profile and increasing empirical clinical use, it was the fifth drug tested by Operation Brain Trauma Therapy (OBTT). We assessed the efficacy of a single 15 min post-injury intravenous (IV) dose (54 or 170 mg/kg) on behavioral, histopathological, and biomarker outcomes after parasagittal fluid percussion brain injury (FPI), controlled cortical impact (CCI), and penetrating ballistic-like brain injury (PBBI) in rats. In FPI, there was no benefit on motor function, but on Morris water maze (MWM), both doses improved latencies and path lengths versus vehicle (p < 0.05). On probe trial, the vehicle group was impaired versus sham, but both LEV treated groups did not differ versus sham, and the 54 mg/kg group was improved versus vehicle (p < 0.05). No histological benefit was seen. In CCI, there was a benefit on beam balance at 170 mg/kg (p < 0.05 vs. vehicle). On MWM, the 54 mg/kg dose was improved and not different from sham. Probe trial did not differ between groups for either dose. There was a reduction in hemispheric tissue loss (p < 0.05 vs. vehicle) with 170 mg/kg. In PBBI, there was no motor, cognitive, or histological benefit from either dose. Regarding biomarkers, in CCI, 24 h glial fibrillary acidic protein (GFAP) blood levels were lower in the 170 mg/kg group versus vehicle (p < 0.05). In PBBI, GFAP blood levels were increased in vehicle and 170 mg/kg groups versus sham (p < 0.05) but not in the 54 mg/kg group. No treatment effects were seen for ubiquitin C-terminal hydrolase-L1 across models. Early single IV LEV produced multiple benefits in CCI and FPI and reduced GFAP levels in PBBI. LEV achieved 10 points at each dose, is the most promising drug tested thus far by OBTT, and the only drug to improve cognitive outcome in any model. LEV has been advanced to testing in the micropig model in OBTT. PMID:26671550

  18. The Spectrum of Neurobehavioral Sequelae after Repetitive Mild Traumatic Brain Injury: A Novel Mouse Model of Chronic Traumatic Encephalopathy

    PubMed Central

    Plog, Benjamin A.; Dayawansa, Samantha; Chen, Michael; Dashnaw, Matthew L.; Czerniecka, Katarzyna; Walker, Corey T.; Viterise, Tyler; Hyrien, Ollivier; Iliff, Jeffrey J.; Deane, Rashid; Nedergaard, Maiken; Huang, Jason H.

    2014-01-01

    Abstract There has been an increased focus on the neurological sequelae of repetitive mild traumatic brain injury (TBI), particularly neurodegenerative syndromes, such as chronic traumatic encephalopathy (CTE); however, no animal model exists that captures the behavioral spectrum of this phenomenon. We sought to develop an animal model of CTE. Our novel model is a modification and fusion of two of the most popular models of TBI and allows for controlled closed-head impacts to unanesthetized mice. Two-hundred and eighty 12-week-old mice were divided into control, single mild TBI (mTBI), and repetitive mTBI groups. Repetitive mTBI mice received six concussive impacts daily for 7 days. Behavior was assessed at various time points. Neurological Severity Score (NSS) was computed and vestibulomotor function tested with the wire grip test (WGT). Cognitive function was assessed with the Morris water maze (MWM), anxiety/risk-taking behavior with the elevated plus maze, and depression-like behavior with the forced swim/tail suspension tests. Sleep electroencephalogram/electromyography studies were performed at 1 month. NSS was elevated, compared to controls, in both TBI groups and improved over time. Repetitive mTBI mice demonstrated transient vestibulomotor deficits on WGT. Repetitive mTBI mice also demonstrated deficits in MWM testing. Both mTBI groups demonstrated increased anxiety at 2 weeks, but repetitive mTBI mice developed increased risk-taking behaviors at 1 month that persist at 6 months. Repetitive mTBI mice exhibit depression-like behavior at 1 month. Both groups demonstrate sleep disturbances. We describe the neurological sequelae of repetitive mTBI in a novel mouse model, which resemble several of the neuropsychiatric behaviors observed clinically in patients sustaining repetitive mild head injury. PMID:24766454

  19. Molecular mechanisms of cognitive dysfunction following traumatic brain injury

    PubMed Central

    Walker, Kendall R.; Tesco, Giuseppina

    2013-01-01

    Traumatic brain injury (TBI) results in significant disability due to cognitive deficits particularly in attention, learning and memory, and higher-order executive functions. The role of TBI in chronic neurodegeneration and the development of neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic Lateral Sclerosis (ALS) and most recently chronic traumatic encephalopathy (CTE) is of particular importance. However, despite significant effort very few therapeutic options exist to prevent or reverse cognitive impairment following TBI. In this review, we present experimental evidence of the known secondary injury mechanisms which contribute to neuronal cell loss, axonal injury, and synaptic dysfunction and hence cognitive impairment both acutely and chronically following TBI. In particular we focus on the mechanisms linking TBI to the development of two forms of dementia: AD and CTE. We provide evidence of potential molecular mechanisms involved in modulating Aβ and Tau following TBI and provide evidence of the role of these mechanisms in AD pathology. Additionally we propose a mechanism by which Aβ generated as a direct result of TBI is capable of exacerbating secondary injury mechanisms thereby establishing a neurotoxic cascade that leads to chronic neurodegeneration. PMID:23847533

  20. [Hypopituitarism following traumatic brain injury: diagnostic and therapeutic issues].

    PubMed

    Lecoq, A-L; Chanson, P

    2015-10-01

    Traumatic Brain Injury (TBI) is a well-known public health problem worldwide and is a leading cause of death and disability, particularly in young adults. Besides neurological and psychiatric issues, pituitary dysfunction can also occur after TBI, in the acute or chronic phase. The exact prevalence of post-traumatic hypopituitarism is difficult to assess due to the wide heterogeneity of published studies and bias in interpretation of hormonal test results in this specific population. Predictive factors for hypopituitarism have been proposed and are helpful for the screening. The pathophysiology of pituitary dysfunction after TBI is not well understood but the vascular hypothesis is privileged. Activation of pituitary stem/progenitor cells is probably involved in the recovery of pituitary functions. Those cells also play a role in the induction of pituitary tumors, highlighting their crucial place in pituitary conditions. This review updates the current data related to anterior pituitary dysfunction after TBI and discusses the bias and difficulties encountered in its diagnosis. PMID:26776284

  1. Neurosensory Symptom Complexes after Acute Mild Traumatic Brain Injury

    PubMed Central

    Szczupak, Mikhaylo; Kiderman, Alexander; Crawford, James; Murphy, Sara; Marshall, Kathryn; Pelusso, Constanza

    2016-01-01

    Mild Traumatic Brain Injury (mTBI) is a prominent public health issue. To date, subjective symptom complaints primarily dictate diagnostic and treatment approaches. As such, the description and qualification of these symptoms in the mTBI patient population is of great value. This manuscript describes the symptoms of mTBI patients as compared to controls in a larger study designed to examine the use of vestibular testing to diagnose mTBI. Five symptom clusters were identified: Post-Traumatic Headache/Migraine, Nausea, Emotional/Affective, Fatigue/Malaise, and Dizziness/Mild Cognitive Impairment. Our analysis indicates that individuals with mTBI have headache, dizziness, and cognitive dysfunction far out of proportion to those without mTBI. In addition, sleep disorders and emotional issues were significantly more common amongst mTBI patients than non-injured individuals. A simple set of questions inquiring about dizziness, headache, and cognitive issues may provide diagnostic accuracy. The consideration of other symptoms may be critical for providing prognostic value and treatment for best short-term outcomes or prevention of long-term complications. PMID:26727256

  2. Hypothalamic-Pituitary Autoimmunity and Traumatic Brain Injury

    PubMed Central

    Guaraldi, Federica; Grottoli, Silvia; Arvat, Emanuela; Ghigo, Ezio

    2015-01-01

    Background: Traumatic brain injury (TBI) is a leading cause of secondary hypopituitarism in children and adults, and is responsible for impaired quality of life, disabilities and compromised development. Alterations of pituitary function can occur at any time after the traumatic event, presenting in various ways and evolving during time, so they require appropriate screening for early detection and treatment. Although the exact pathophysiology is unknown, several mechanisms have been hypothesized, including hypothalamic-pituitary autoimmunity (HP-A). The aim of this study was to systematically review literature on the association between HP-A and TBI-induced hypopituitarism. Major pitfalls related to the HP-A investigation were also discussed. Methods: The PubMed database was searched with a string developed for this purpose, without temporal or language limits, for original articles assessing the association of HP-A and TBI-induced hypopituitarism. Results: Three articles from the same group met the inclusion criteria. Anti-pituitary and anti-hypothalamic antibodies were detected using indirect immunofluorescence in a significant number of patients with acute and chronic TBI. Elevated antibody titer was associated with an increased risk of persistent hypopituitarism, especially somatotroph and gonadotroph deficiency, while no correlations were found with clinical parameters. Conclusion: HPA seems to contribute to TBI-induced pituitary damage, although major methodological issues need to be overcome and larger studies are warranted to confirm these preliminary data. PMID:26239463

  3. Preventable deaths in patients with traumatic brain injury

    PubMed Central

    Kim, Seong Chun; Song, Kyoung Jun; Shin, Sang Do; Lee, Seung Chul; Park, Ju Ok; Holmes, James F.

    2015-01-01

    Objective The objective of this study is to evaluate the rate of and etiology for preventable deaths in patients with traumatic brain injuries (TBIs). Methods We conducted a retrospective, multicenter review of patients with TBIs who died within 7 days of their traumatic event from June 2008 to May 2009. Three board certified emergency physicians independently reviewed every case using a structured survey format. Cases were considered preventable deaths only if all physicians independently agreed the death was preventable. Management errors contributing to the preventable death were determined. Results Forty-one patients who died from TBI were eligible. Preventable deaths were identified in nine (22%; 95% confidence interval [CI], 11 to 28) cases. Fifty-six management errors were identified including 36 (64%; 95% CI, 50 to 77) in the emergency department and 13 (23%; 95% CI, 13 to 36) in the prehospital phase. Thirty (54%; 95% CI, 40 to 67) management errors were process-related, and 26 (46%; 95% CI, 33 to 60) were structure-related. Conclusion An important and measurable rate of preventable mortality occurs in the initial care of TBI patients. Errors were common and most occurred in the emergency department. In addition, errors were common in the prehospital phase but did not always lead to mortality. When analyzed by type of problem, both process-related and structure-related errors occurred in similar proportions.

  4. A review of glutamate's role in traumatic brain injury mechanisms

    NASA Astrophysics Data System (ADS)

    Good, Cameron H.

    2013-05-01

    Glutamate is the primary excitatory neurotransmitter used by the central nervous system (CNS) for synaptic communication, and its extracellular concentration is tightly regulated by glutamate transporters located on nearby astrocytes. Both animal models and human clinical studies have demonstrated elevated glutamate levels immediately following a traumatic brain event, with the duration and severity of the rise corresponding to prognosis. This rise in extracellular glutamate likely results from a combination of excessive neurotransmitter release from damaged neurons and down regulation of uptake mechanisms in local astrocytes. The immediate results of a traumatic event can lead to necrotic tissue in severely injured regions, while prolonged increases in excitatory transmission can cause secondary excitotoxic injury through activation of delayed apoptotic pathways. Initial TBI animal studies utilized a variety of broad glutamate receptor antagonists to successfully combat secondary injury mechanisms, but unfortunately this same strategy has proven inconclusive in subsequent human trials due to deleterious side effects and heterogeneity of injuries. More recent treatment strategies have utilized specific glutamate receptor subunit antagonists in an effort to minimize side effects and have shown promising results. Future challenges will be detecting the concentration and kinetics of the glutamate rise following injury, determining which patient populations could benefit from antagonist treatment based on their extracellular glutamate concentrations and when drugs should be administered to maximize efficacy.

  5. Impact Acceleration Model of Diffuse Traumatic Brain Injury.

    PubMed

    Hellewell, Sarah C; Ziebell, Jenna M; Lifshitz, Jonathan; Morganti-Kossmann, M Cristina

    2016-01-01

    The impact acceleration (I/A) model of traumatic brain injury (TBI) was developed to reliably induce diffuse traumatic axonal injury in rats in the absence of skull fractures and parenchymal focal lesions. This model replicates a pathophysiology that is commonly observed in humans with diffuse axonal injury (DAI) caused by acceleration-deceleration forces. Such injuries are typical consequences of motor vehicle accidents and falls, which do not necessarily require a direct impact to the closed skull. There are several desirable characteristics of the I/A model, including the extensive axonal injury produced in the absence of a focal contusion, the suitability for secondary insult modeling, and the adaptability for mild/moderate injury through alteration of height and/or weight. Furthermore, the trauma device is inexpensive and readily manufactured in any laboratory, and the induction of injury is rapid (~45 min per animal from weighing to post-injury recovery) allowing multiple animal experiments per day. In this chapter, we describe in detail the methodology and materials required to produce the rat model of I/A in the laboratory. We also review current adaptations to the model to alter injury severity, discuss frequent complications and technical issues encountered using this model, and provide recommendations to ensure technically sound injury induction. PMID:27604723

  6. Oculomotor, Vestibular, and Reaction Time Tests in Mild Traumatic Brain Injury

    PubMed Central

    Szczupak, Mikhaylo; Snapp, Hillary; Crawford, James; Murphy, Sara; Marshall, Kathryn; Pelusso, Constanza; Knowles, Sean; Kiderman, Alex

    2016-01-01

    Objective Mild traumatic brain injury is a major public health issue and is a particular concern in sports. One of the most difficult issues with respect to mild traumatic brain injury involves the diagnosis of the disorder. Typically, diagnosis is made by a constellation of physical exam findings. However, in order to best manage mild traumatic brain injury, it is critically important to develop objective tests that substantiate the diagnosis. With objective tests the disorder can be better characterized, more accurately diagnosed, and studied more effectively. In addition, prevention and treatments can be applied where necessary. Methods Two cohorts each of fifty subjects with mild traumatic brain injury and one hundred controls were evaluated with a battery of oculomotor, vestibular and reaction time related tests applied to a population of individuals with mild traumatic brain injury as compared to controls. Results We demonstrated pattern differences between the two groups and showed how three of these tests yield an 89% sensitivity and 95% specificity for confirming a current diagnosis of mild traumatic brain injury. Interpretation These results help better characterize the oculomotor, vestibular, and reaction time differences between those the mild traumatic brain injury and non-affected individuals. This characterization will allow for the development of more effective point of care neurologic diagnostic techniques and allow for more targeted treatment which may allow for quicker return to normal activity. PMID:27654131

  7. Use and Effect of Vasopressors after Pediatric Traumatic Brain Injury

    PubMed Central

    Di Gennaro, Jane L.; Mack, Christopher D.; Malakouti, Amin; Zimmerman, Jerry J.; Armstead, William; Vavilala, Monica S.

    2011-01-01

    Background Vasopressors are commonly used to increase mean arterial blood pressure (MAP) and cerebral perfusion pressure (CPP) after traumatic brain injury (TBI), but there are few data comparing vasopressor effectiveness after pediatric TBI. Objective: To determine which vasopressor is most effective at increasing MAP and CPP in children with moderate-to-severe TBI. Methods After institutional review board approval, we performed a retrospective cohort study of children 0–17 years old admitted to a level 1 trauma center (Harborview Medical Center, Seattle, Wash., USA) between 2002 and 2007 with moderate-to-severe TBI who received a vasopressor to increase blood pressure. Baseline demographic and physiologic characteristics and hourly physiologic monitoring for 3 h after having started a vasopressor were abstracted. We evaluated differences in MAP and CPP at 3 h after initiation of therapy between phenylephrine, dopamine and norepinephrine among patients who did not require a second vasopressor during this time. Multivariate linear regression was used to adjust for age, gender, injury severity score and baseline MAP or CPP and to cluster by subject. Results Eighty-two patients contributed data to the entire dataset. The most common initial medication was phenylephrine for 47 (57%). Patients receiving phenylephrine and norepinephrine tended to be older than those receiving dopamine and epinephrine. Thirteen (16%) of the patients received a second vasopressor during the first 3 h of treatment and were thus not included in the regression analyses; these patients received more fluid resuscitation and exhibited higher in-hospital mortality (77 vs. 32%; p = 0.004) compared to patients receiving a single vasopressor. The norepinephrine group exhibited a 5 mm Hg higher MAP (95% CI: −4 to 13; p = 0.31) and a 12 mm Hg higher CPP (95% CI: −2 to 26; p = 0.10) than the phenylephrine group, and a 5 mm Hg higher MAP (95% CI: −4 to 15; p = 0.27) and a 10 mm Hg higher CPP

  8. Brain stimulation: Neuromodulation as a potential treatment for motor recovery following traumatic brain injury☆

    PubMed Central

    Clayton, E.; Kinley-Cooper, S.K.; Weber, R.A.; Adkins, D.L.

    2016-01-01

    There is growing evidence that electrical and magnetic brain stimulation can improve motor function and motor learning following brain damage. Rodent and primate studies have strongly demonstrated that combining cortical stimulation (CS) with skilled motor rehabilitative training enhances functional motor recovery following stroke. Brain stimulation following traumatic brain injury (TBI) is less well studied, but early pre-clinical and human pilot studies suggest that it is a promising treatment for TBI-induced motor impairments as well. This review will first discuss the evidence supporting brain stimulation efficacy derived from the stroke research field as proof of principle and then will review the few studies exploring neuromodulation in experimental TBI studies. PMID:26855256

  9. Specificity of Cognitive and Behavioral Complaints in Post-Traumatic Stress Disorder and Mild Traumatic Brain Injury

    PubMed Central

    Pineau, Hélène; Marchand, André; Guay, Stéphane

    2015-01-01

    Characterization of cognitive and behavioral complaints is explored in Post-traumatic stress disorder (PTSD) and mild traumatic brain injury (MTBI) samples according to the severity of PTSD, depression and general anxiety conditions. Self-reported questionnaires on cognitive and behavioral changes are administered to PTSD, MTBI, MTBI/PTSD and control groups. Confounding variables are controlled. All groups report more complaints since the traumatic event. PTSD and MTBI/PTSD groups report more anxiety symptoms, depression and complaints compared to the MTBI group. Relatives of the PTSD group confirm most of the behavioral changes reported. Results suggest the utility of self-reported questionnaires to personalize cognitive and behavioral interventions in PTSD and MTBI to cope with the impacts of the traumatic event. PMID:25646994

  10. Biomechanical Risk Estimates for Mild Traumatic Brain Injury

    PubMed Central

    Funk, J. R.; Duma, S. M.; Manoogian, S. J.; Rowson, S.

    2007-01-01

    The objective of this study was to characterize the risk of mild traumatic brain injury (MTBI) in living humans based on a large set of head impact data taken from American football players at the collegiate level. Real-time head accelerations were recorded from helmet-mounted accelerometers designed to stay in contact with the player’s head. Over 27,000 head impacts were recorded, including four impacts resulting in MTBI. Parametric risk curves were developed by normalizing MTBI incidence data by head impact exposure data. An important finding of this research is that living humans, at least in the setting of collegiate football, sustain much more significant head impacts without apparent injury than previously thought. The following preliminary nominal injury assessment reference values associated with a 10% risk of MTBI are proposed: a peak linear head acceleration of 165 g, a HIC of 400, and a peak angular head acceleration of 9000 rad/s2. PMID:18184501

  11. Traumatic Brain Injury and Olfaction: A Systematic Review

    PubMed Central

    Schofield, Peter William; Moore, Tammie Maree; Gardner, Andrew

    2014-01-01

    Traumatic brain injury (TBI) is a common condition that is often complicated by neuropsychiatric sequelae that can have major impacts on function and quality of life. An alteration in the sense of smell is recognized as a relatively common complication of TBI; however in clinical practice, this complication may not be sought or adequately characterized. We conducted a systematic review of studies concerned with olfactory functioning following TBI. Our predetermined criteria led to the identification of 25 studies published in English, which we examined in detail. We have tabulated the data from these studies in eight separate tables, beginning with Table 1, which highlights each study’s key findings, and we provide a summary/synthesis of the findings in the accompanying results and discussion sections. Despite widely differing methodologies, the studies attest to a high frequency of post-TBI olfactory dysfunction and indicate that its presence can serve as a potential marker of additional structural or functional morbidities. PMID:24478752

  12. Effect of Preferred Music on Agitation After Traumatic Brain Injury.

    PubMed

    Park, Soohyun; Williams, Reg Arthur; Lee, Donghyun

    2016-04-01

    Agitation is a common behavioral problem after traumatic brain injury (TBI), which threatens the safety of patients and caregivers and disrupts the rehabilitation process. This study aimed to evaluate the effects of a preferred music intervention on the reduction of agitation in TBI patients and to compare the effects of preferred music with those of classical "relaxation" music. A single group, within-subjects, randomized crossover trial design was formed, consisting of 14 agitated patients with cognitive impairment after severe TBI. Patients listened to preferred music and classical "relaxation" music, with a wash-out period in between. Patients listening to the preferred music reported a significantly greater reduction in agitation compared with the effect seen during the classical "relaxation" music intervention (p = .046). These findings provide preliminary evidence that the preferred music intervention may be effective as an environmental therapeutic approach for reducing agitation after TBI.

  13. Proteomics: in pursuit of effective traumatic brain injury therapeutics

    PubMed Central

    Lizhnyak, Pavel N.; Ottens, Andrew K.

    2015-01-01

    Summary Effective traumatic brain injury (TBI) therapeutics remain stubbornly elusive. Efforts in the field have been challenged by the heterogeneity of clinical TBI, with greater complexity among underlying molecular phenotypes than initially conceived. Future research must confront the multitude of factors comprising this heterogeneity, representing a big data challenge befitting the coming informatics age. Proteomics is poised to serve a central role in prescriptive therapeutic development, as it offers an efficient endpoint within which to assess post-TBI biochemistry. We examine rationale for multifactor TBI proteomic studies and the particular importance of temporal profiling in defining biochemical sequences and guiding therapeutic development. Lastly, we offer perspective on repurposing biofluid proteomics to develop theragnostic assays with which to prescribe, monitor and assess pharmaceutics for improved translation and outcome for TBI patients. PMID:25603864

  14. Structural Neuroimaging Findings in Mild Traumatic Brain Injury.

    PubMed

    Bigler, Erin D; Abildskov, Tracy J; Goodrich-Hunsaker, Naomi J; Black, Garrett; Christensen, Zachary P; Huff, Trevor; Wood, Dawn-Marie G; Hesselink, John R; Wilde, Elisabeth A; Max, Jeffrey E

    2016-09-01

    Common neuroimaging findings in mild traumatic brain injury (mTBI), including sport-related concussion (SRC), are reviewed based on computed tomography and magnetic resonance imaging (MRI). Common abnormalities radiologically identified on the day of injury, typically a computed tomographic scan, are in the form of contusions, small subarachnoid or intraparenchymal hemorrhages as well as subdural and epidural collections, edema, and skull fractures. Common follow-up neuroimaging findings with MRI include white matter hyperintensities, hypointense signal abnormalities that reflect prior hemorrhage, focal encephalomalacia, presence of atrophy and/or dilated Virchow-Robins perivascular space. The MRI findings from a large pediatric mTBI study show low frequency of positive MRI findings at 6 months postinjury. The review concludes with an examination of some of the advanced MRI-based image analysis methods that can be performed in the patient who has sustained an mTBI. PMID:27482782

  15. Genetic predictors of outcome following traumatic brain injury.

    PubMed

    Lipsky, Robert H; Lin, Mingkuan

    2015-01-01

    The nature of traumatic brain injury (TBI) has acute and chronic outcomes for those who survive. Over time, the chronic process of injury impacts multiple organ systems that may lead to disease. We discuss possible mechanisms and methodological issues in the context of candidate gene association studies using TBI patient populations. Because study population sizes have been generally limited, we discussed results on genes that have been the focus of independent studies. We also present a justification for testing more speculative candidate genes in recovery from TBI, such as those involved in circadian rhythm, to outline the importance of prioritizing functional variants in genes that may modulate recovery or provide neuroprotection from TBI. Finally, we provide a perspective on how future research will integrate population level genetic findings with the biological basis of disease in order to create a resource of predictive outcome measures for individual patients.

  16. Clinical Traumatic Brain Injury in the Preclinical Setting.

    PubMed

    Berkner, Justin; Mannix, Rebekah; Qiu, Jianhua

    2016-01-01

    Traumatic brain injury (TBI) is the leading cause of death and disability for people under 45 years of age. Clinical TBI is often the result of disparate forces resulting in heterogeneous injuries. Preclinical modeling of TBI is a vital tool for studying the complex cascade of metabolic, cellular, and molecular post-TBI events collectively termed secondary injury. Preclinical models also provide an important platform for studying therapeutic interventions. However, modeling TBI in the preclinical setting is challenging, and most models replicate only certain aspects of clinical TBI. This chapter details the most widely used models of preclinical TBI, including the controlled cortical impact, fluid percussion, blast, and closed head models. Each of these models replicates particular critical aspects of clinical TBI. Prior to selecting a preclinical TBI model, it is important to address what aspect of human TBI is being sought to evaluate. PMID:27604710

  17. Neuropsychology of Neuroendocrine Dysregulation after Traumatic Brain Injury.

    PubMed

    Zihl, Josef; Almeida, Osborne F X

    2015-05-20

    Endocrine dysfunction is a common effect of traumatic brain injury (TBI). In addition to affecting the regulation of important body functions, the disruption of endocrine physiology can significantly impair mental functions, such as attention, memory, executive function, and mood. This mini-review focuses on alterations in mental functioning that are associated with neuroendocrine disturbances in adults who suffered TBI. It summarizes the contribution of hormones to the regulation of mental functions, the consequences of TBI on mental health and neuroendocrine homeostasis, and the effects of hormone substitution on mental dysfunction caused by TBI. The available empirical evidence suggests that comprehensive assessment of mental functions should be standard in TBI subjects presenting with hormone deficiency and that hormone replacement therapy should be accompanied by pre- and post-assessments.

  18. Chapter 2 traumatic brain injury research in military populations.

    PubMed

    Kasper, Christine E

    2015-01-01

    Traumatic brain injury (TBI) in all of its forms--blast, concussive, and penetrating--has been an unfortunate sequela of warfare since ancient times. The continued evolution of military munitions and armor on the battlefield, as well as the insurgent use of improvised explosive devices, has led to blast-related TBI whose long-term effects on behavior and cognition are not yet known. Advances in medical care have greatly increased survival from these types of injuries. Therefore, an understanding of the potential health effects of TBI is essential. This review focuses on specific aspects of military-related TBI. There exists a large body of literature reporting the environmental conditions, forces, and staging of injury. Many of these studies are focused on the neuropathology of TBI, due to blast overpressure waves, and the emergence of large numbers of mild blast-related TBI cases. PMID:25946382

  19. Initial management of traumatic brain injury in the rural setting.

    PubMed

    Honeybul, Stephen; Woods, Paul

    2013-01-01

    Healthcare workers in the rural setting face unique problems when dealing with head injured patients however the basic principle of medical management are the same in any situation. The key initial elements remain aggressive early resuscitation followed by a comprehensive assessment of conscious level and either early consultation or transfer to a neurosurgical facility. What has improved considerably over recent years is the understanding of the pathophysiology of traumatic brain injury and as such some of the medical management strategies have changed. A basic understanding of some of these concepts is useful in the clinical setting and serves to emphasis the importance of effective early medical management. Thereafter consideration must be given to which patients require radiological investigations and possible discussion with or transfer to a neurosurgical facility.

  20. Pharmacology of traumatic brain injury: where is the "golden bullet"?

    PubMed

    Beauchamp, Kathryn; Mutlak, Haitham; Smith, Wade R; Shohami, Esther; Stahel, Philip F

    2008-01-01

    Traumatic brain injury (TBI) represents a major health care problem and a significant socioeconomic challenge worldwide. In the United States alone, approximately 1.5 million patients are affected each year, and the mortality of severe TBI remains as high as 35%-40%. These statistics underline the urgent need for efficient treatment modalities to improve posttraumatic morbidity and mortality. Despite advances in basic and clinical research as well as improved neurological intensive care in recent years, no specific pharmacological therapy for TBI is available that would improve the outcome of these patients. Understanding of the cellular and molecular mechanisms underlying the pathophysiological events after TBI has resulted in the identification of new potential therapeutic targets. Nevertheless, the extrapolation from basic research data to clinical application in TBI patients has invariably failed, and results from prospective clinical trials are disappointing. We review the published prospective clinical trials on pharmacological treatment modalities for TBI patients and outline future promising therapeutic avenues in the field.

  1. Structural Neuroimaging Findings in Mild Traumatic Brain Injury.

    PubMed

    Bigler, Erin D; Abildskov, Tracy J; Goodrich-Hunsaker, Naomi J; Black, Garrett; Christensen, Zachary P; Huff, Trevor; Wood, Dawn-Marie G; Hesselink, John R; Wilde, Elisabeth A; Max, Jeffrey E

    2016-09-01

    Common neuroimaging findings in mild traumatic brain injury (mTBI), including sport-related concussion (SRC), are reviewed based on computed tomography and magnetic resonance imaging (MRI). Common abnormalities radiologically identified on the day of injury, typically a computed tomographic scan, are in the form of contusions, small subarachnoid or intraparenchymal hemorrhages as well as subdural and epidural collections, edema, and skull fractures. Common follow-up neuroimaging findings with MRI include white matter hyperintensities, hypointense signal abnormalities that reflect prior hemorrhage, focal encephalomalacia, presence of atrophy and/or dilated Virchow-Robins perivascular space. The MRI findings from a large pediatric mTBI study show low frequency of positive MRI findings at 6 months postinjury. The review concludes with an examination of some of the advanced MRI-based image analysis methods that can be performed in the patient who has sustained an mTBI.

  2. Persistent cognitive dysfunction after traumatic brain injury: A dopamine hypothesis

    PubMed Central

    Bales, James W.; Wagner, Amy K.; Kline, Anthony E.; Dixon, C. Edward

    2010-01-01

    Traumatic brain injury (TBI) represents a significant cause of death and disability in industrialized countries. Of particular importance to patients the chronic effect that TBI has on cognitive function. Therapeutic strategies have been difficult to evaluate because of the complexity of injuries and variety of patient presentations within a TBI population. However, pharmacotherapies targeting dopamine (DA) have consistently shown benefits in attention, behavioral outcome, executive function, and memory. Still it remains unclear what aspect of TBI pathology is targeted by DA therapies and what time-course of treatment is most beneficial for patient outcomes. Fortunately, ongoing research in animal models has begun to elucidate the pathophysiology of DA alterations after TBI. The purpose of this review is to discuss clinical and experimental research examining DAergic therapies after TBI, which will in turn elucidate the importance of DA for cognitive function/dysfunction after TBI as well as highlight the areas that require further study. PMID:19580914

  3. Persistent vertigo and dizziness after mild traumatic brain injury.

    PubMed

    Fife, Terry D; Kalra, Deepak

    2015-04-01

    Vertigo, dizziness, and disequilibrium are common symptoms following concussion or mild traumatic brain injury (mTBI). Dizziness and vertigo may be the result of trauma to the peripheral vestibular system or the central nervous system, or, in some cases, may be due to anxiety, depression, or posttraumatic stress disorder; these mechanisms are not mutually exclusive. While most peripheral vestibular disorders can be identified by testing and examination, those without inner-ear causes that have persisting complaints of dizziness and motion sickness are more difficult to understand and to manage. Some of these patients exhibit features compatible with vestibular migraine and may be treated successfully with migraine-preventative medications. This paper reviews the nonotogenic causes of persisting dizziness, the possible mechanisms, and the pathophysiology, as a framework for patient management and for future research.

  4. Recovery of educational skills following paediatric traumatic brain injury.

    PubMed

    Catroppa, C; Anderson, V

    1999-01-01

    Academic success in the classroom is often dependent upon a child's ability in the areas of literacy, such as reading and spelling, and arithmetic. Following traumatic brain injury these skills are often compromised. The present study examined the recovery of educational skills (reading accuracy, reading comprehension, spelling and arithmetic) over 24 months post-injury, in a group of children who had sustained a mild, moderate or severe TBI. Results showed that the severe TBI group exhibited greater deficits on reading comprehension and arithmetic, while the moderate and severe TBI groups performed similarly in the areas of reading accuracy and spelling. Future research is required to further investigate predictors of educational outcome post-TBI. PMID:10819429

  5. A new avenue for lithium: intervention in traumatic brain injury.

    PubMed

    Leeds, Peter R; Yu, Fengshan; Wang, Zhifei; Chiu, Chi-Tso; Zhang, Yumin; Leng, Yan; Linares, Gabriel R; Chuang, De-Maw

    2014-06-18

    Traumatic brain injury (TBI) is a leading cause of disability and death from trauma to central nervous system (CNS) tissues. For patients who survive the initial injury, TBI can lead to neurodegeneration as well as cognitive and motor deficits, and is even a risk factor for the future development of neurodegenerative disorders such as Alzheimer's disease. Preclinical studies of multiple neuropathological and neurodegenerative disorders have shown that lithium, which is primarily used to treat bipolar disorder, has considerable neuroprotective effects. Indeed, emerging evidence now suggests that lithium can also mitigate neurological deficits incurred from TBI. Lithium exerts neuroprotective effects and stimulates neurogenesis via multiple signaling pathways; it inhibits glycogen synthase kinase-3 (GSK-3), upregulates neurotrophins and growth factors (e.g., brain-derived neurotrophic factor (BDNF)), modulates inflammatory molecules, upregulates neuroprotective factors (e.g., B-cell lymphoma-2 (Bcl-2), heat shock protein 70 (HSP-70)), and concomitantly downregulates pro-apoptotic factors. In various experimental TBI paradigms, lithium has been shown to reduce neuronal death, microglial activation, cyclooxygenase-2 induction, amyloid-β (Aβ), and hyperphosphorylated tau levels, to preserve blood-brain barrier integrity, to mitigate neurological deficits and psychiatric disturbance, and to improve learning and memory outcome. Given that lithium exerts multiple therapeutic effects across an array of CNS disorders, including promising results in preclinical models of TBI, additional clinical research is clearly warranted to determine its therapeutic attributes for combating TBI. Here, we review lithium's exciting potential in ameliorating physiological as well as cognitive deficits induced by TBI.

  6. Screening for Traumatic Brain Injury: Findings and Public Health Implications

    PubMed Central

    Dams-O’Connor, Kristen; Cantor, Joshua B.; Brown, Margaret; Dijkers, Marcel P.; Spielman, Lisa A.; Gordon, Wayne A.

    2016-01-01

    Objective To provide an overview of a series of projects that used a structured self-report screening tool in diverse settings and samples to screen for lifetime history of traumatic brain injury (TBI). Setting Diverse community settings. Participants Homeless persons (n = 111), individuals with HIV seeking vocational rehabilitation (n = 173), youth in the juvenile justice system (n = 271), public schoolchildren (n = 174), substance users (n = 845), intercollegiate athletes (n = 90), and other community-based samples (n = 396). Design Cross-sectional. Main Measure Brain Injury Screening Questionnaire. Results Screening using the Brain Injury Screening Questionnaire finds that 27% to 54% of those in high-risk populations report a history of TBI with chronic symptoms. Associations between TBI and social, academic, or other problems are evident in several studies. In non–high-risk community samples, 9% to 12% of individuals report TBI with chronic symptoms. Conclusion Systematic TBI screening can be implemented efficiently and inexpensively in a variety of settings. Lifetime TBI history data gathered using a structured self-report instrument can augment existing estimates of the prevalence of TBI, both as an acute event and as a chronic condition. Identification of individuals with TBI can facilitate primary prevention efforts, such as reducing risk for reinjury in high-risk groups, and provide access to appropriate interventions that can reduce the personal and societal costs of TBI (tertiary prevention). PMID:25370440

  7. Normobaric oxygen worsens outcome after a moderate traumatic brain injury.

    PubMed

    Talley Watts, Lora; Long, Justin Alexander; Manga, Venkata Hemanth; Huang, Shiliang; Shen, Qiang; Duong, Timothy Q

    2015-07-01

    Traumatic brain injury (TBI) is a multifaceted injury and a leading cause of death in children, young adults, and increasingly in Veterans. However, there are no neuroprotective agents clinically available to counteract damage or promote repair after brain trauma. This study investigated the neuroprotective effects of normobaric oxygen (NBO) after a controlled cortical impact in rats. The central hypothesis was that NBO treatment would reduce lesion volume and functional deficits compared with air-treated animals after TBI by increasing brain oxygenation thereby minimizing ischemic injury. In a randomized double-blinded design, animals received either NBO (n = 8) or normal air (n = 8) after TBI. Magnetic resonance imaging (MRI) was performed 0 to 3 hours, and 1, 2, 7, and 14 days after an impact to the primary forelimb somatosensory cortex. Behavioral assessments were performed before injury induction and before MRI scans on days 2, 7, and 14. Nissl staining was performed on day 14 to corroborate the lesion volume detected from MRI. Contrary to our hypothesis, we found that NBO treatment increased lesion volume in a rat model of moderate TBI and had no positive effect on behavioral measures. Our results do not promote the acute use of NBO in patients with moderate TBI. PMID:25690469

  8. Neuroprotective measures in children with traumatic brain injury.

    PubMed

    Agrawal, Shruti; Branco, Ricardo Garcia

    2016-02-01

    Traumatic brain injury (TBI) is a major cause of death and disability in children. Severe TBI is a leading cause of death and often leads to life changing disabilities in survivors. The modern management of severe TBI in children on intensive care unit focuses on preventing secondary brain injury to improve outcome. Standard neuroprotective measures are based on management of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) to optimize the cerebral blood flow and oxygenation, with the intention to avoid and minimise secondary brain injury. In this article, we review the current trends in management of severe TBI in children, detailing the general and specific measures followed to achieve the desired ICP and CPP goals. We discuss the often limited evidence for these therapeutic interventions in children, extrapolation of data from adults, and current recommendation from paediatric guidelines. We also review the recent advances in understanding the intracranial physiology and neuroprotective therapies, the current research focus on advanced and multi-modal neuromonitoring, and potential new therapeutic and prognostic targets. PMID:26855892

  9. Normobaric oxygen worsens outcome after a moderate traumatic brain injury.

    PubMed

    Talley Watts, Lora; Long, Justin Alexander; Manga, Venkata Hemanth; Huang, Shiliang; Shen, Qiang; Duong, Timothy Q

    2015-07-01

    Traumatic brain injury (TBI) is a multifaceted injury and a leading cause of death in children, young adults, and increasingly in Veterans. However, there are no neuroprotective agents clinically available to counteract damage or promote repair after brain trauma. This study investigated the neuroprotective effects of normobaric oxygen (NBO) after a controlled cortical impact in rats. The central hypothesis was that NBO treatment would reduce lesion volume and functional deficits compared with air-treated animals after TBI by increasing brain oxygenation thereby minimizing ischemic injury. In a randomized double-blinded design, animals received either NBO (n = 8) or normal air (n = 8) after TBI. Magnetic resonance imaging (MRI) was performed 0 to 3 hours, and 1, 2, 7, and 14 days after an impact to the primary forelimb somatosensory cortex. Behavioral assessments were performed before injury induction and before MRI scans on days 2, 7, and 14. Nissl staining was performed on day 14 to corroborate the lesion volume detected from MRI. Contrary to our hypothesis, we found that NBO treatment increased lesion volume in a rat model of moderate TBI and had no positive effect on behavioral measures. Our results do not promote the acute use of NBO in patients with moderate TBI.

  10. Advances in imaging explosive blast mild traumatic brain injury.

    PubMed

    Hetherington, H; Bandak, A; Ling, G; Bandak, F A

    2015-01-01

    In the past, direct physical evidence of mild traumatic brain injury (mTBI) from explosive blast has been difficult to obtain through conventional imaging modalities such as T1- and T2-weighted magnetic resonance imaging (MRI) and computed tomography (CT). Here, we review current progress in detecting evidence of brain injury from explosive blast using advanced imaging, including diffusion tensor imaging (DTI), functional MRI (fMRI), and the metabolic imaging methods such as positron emission tomography (PET) and magnetic resonance spectroscopic imaging (MRSI), where each targets different aspects of the pathology involved in mTBI. DTI provides a highly sensitive measure to detect primary changes in the microstructure of white matter tracts. fMRI enables the measurement of changes in brain activity in response to different stimuli or tasks. Remarkably, all three of these paradigms have found significant success in conventional mTBI where conventional clinical imaging frequently fails to provide definitive differences. Additionally, although used less frequently for conventional mTBI, PET has the potential to characterize a variety of neurotransmitter systems using target agents and will undoubtedly play a larger role, once the basic mechanisms of injury are better understood and techniques to identify the injury are more common. Finally, our MRSI imaging studies, although acquired at much lower spatial resolution, have demonstrated selectivity to different metabolic and physiologic processes, uncovering some of the most profound differences on an individual by individual basis, suggesting the potential for utility in the management of individual patients.

  11. Sleep disruption and the sequelae associated with traumatic brain injury

    PubMed Central

    Lucke-Wold, Brandon P.; Smith, Kelly E.; Nguyen, Linda; Turner, Ryan C.; Logsdon, Aric F.; Jackson, Garrett J.; Huber, Jason D.; Rosen, Charles L.; Miller, Diane B.

    2016-01-01

    Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy. PMID:25956251

  12. Normobaric oxygen worsens outcome after a moderate traumatic brain injury

    PubMed Central

    Talley Watts, Lora; Long, Justin Alexander; Manga, Venkata Hemanth; Huang, Shiliang; Shen, Qiang; Duong, Timothy Q

    2015-01-01

    Traumatic brain injury (TBI) is a multifaceted injury and a leading cause of death in children, young adults, and increasingly in Veterans. However, there are no neuroprotective agents clinically available to counteract damage or promote repair after brain trauma. This study investigated the neuroprotective effects of normobaric oxygen (NBO) after a controlled cortical impact in rats. The central hypothesis was that NBO treatment would reduce lesion volume and functional deficits compared with air-treated animals after TBI by increasing brain oxygenation thereby minimizing ischemic injury. In a randomized double-blinded design, animals received either NBO (n=8) or normal air (n=8) after TBI. Magnetic resonance imaging (MRI) was performed 0 to 3 hours, and 1, 2, 7, and 14 days after an impact to the primary forelimb somatosensory cortex. Behavioral assessments were performed before injury induction and before MRI scans on days 2, 7, and 14. Nissl staining was performed on day 14 to corroborate the lesion volume detected from MRI. Contrary to our hypothesis, we found that NBO treatment increased lesion volume in a rat model of moderate TBI and had no positive effect on behavioral measures. Our results do not promote the acute use of NBO in patients with moderate TBI. PMID:25690469

  13. Child and adolescent traumatic brain injury: correlates of injury severity.

    PubMed

    Max, J E; Lindgren, S D; Knutson, C; Pearson, C S; Ihrig, D; Welborn, A

    1998-01-01

    A record review focused on children and adolescents, with a history of traumatic brain injury, who were consecutively admitted to a brain injury clinic in which all new patients are psychiatrically evaluated. Significant correlates of severity of injury in the cognitive, education and communication domains of functioning included Performance IQ but not Verbal IQ nor standardized ratings of language or learning disability. Current organic personality syndrome (OPS) but not attention deficit hyperactivity disorder or oppositional defiant disorder/conduct disorder diagnostic status was significantly related to severity. In conclusion, the findings in this referred sample are similar to prospective studies indicating that Performance IQ appears sensitive in reflecting brain damage. The finding linking OPS to severity of injury is not surprising. This is because OPS is a diagnosis which is dependent on the clinician's judgment of the likelihood that the organic factor is etiologically related to a defined behavioural syndrome. The diagnosis therefore requires a clinical judgment that the threshold of severity of a presumed organic etiological factor has been reached.

  14. The blood-brain barrier as a target in traumatic brain injury treatment.

    PubMed

    Thal, Serge C; Neuhaus, Winfried

    2014-11-01

    Traumatic brain injury (TBI) is one of the most frequent causes of death in the young population. Several clinical trials have unsuccessfully focused on direct neuroprotective therapies. Recently immunotherapeutic strategies shifted into focus of translational research in acute CNS diseases. Cross-talk between activated microglia and blood-brain barrier (BBB) could initiate opening of the BBB and subsequent recruitment of systemic immune cells and mediators into the brain. Stabilization of the BBB after TBI could be a promising strategy to limit neuronal inflammation, secondary brain damage and acute neurodegeneration. This review provides an overview on the pathophysiology of TBI and brain edema formation including definitions and classification of TBI, current clinical treatment strategies, as well as current understanding on the underlying cellular processes. A summary of in vivo and in vitro models to study different aspects of TBI is presented. Three mechanisms proposed for stabilization of the BBB, myosin light chain kinases, glucocorticoid receptors and peroxisome proliferator-activated receptors are reviewed for their influence on barrier-integrity and outcome after TBI. In conclusion, the BBB is recommended as a promising target for the treatment of traumatic brain injury, and it is suggested that a combination of BBB stabilization and neuroprotectants may improve therapeutic success. PMID:25446615

  15. Glycolysis and the significance of lactate in traumatic brain injury.

    PubMed

    Carpenter, Keri L H; Jalloh, Ibrahim; Hutchinson, Peter J

    2015-01-01

    In traumatic brain injury (TBI) patients, elevation of the brain extracellular lactate concentration and the lactate/pyruvate ratio are well-recognized, and are associated statistically with unfavorable clinical outcome. Brain extracellular lactate was conventionally regarded as a waste product of glucose, when glucose is metabolized via glycolysis (Embden-Meyerhof-Parnas pathway) to pyruvate, followed by conversion to lactate by the action of lactate dehydrogenase, and export of lactate into the extracellular fluid. In TBI, glycolytic lactate is ascribed to hypoxia or mitochondrial dysfunction, although the precise nature of the latter is incompletely understood. Seemingly in contrast to lactate's association with unfavorable outcome is a growing body of evidence that lactate can be beneficial. The idea that the brain can utilize lactate by feeding into the tricarboxylic acid (TCA) cycle of neurons, first published two decades ago, has become known as the astrocyte-neuron lactate shuttle hypothesis. Direct evidence of brain utilization of lactate was first obtained 5 years ago in a cerebral microdialysis study in TBI patients, where administration of (13)C-labeled lactate via the microdialysis catheter and simultaneous collection of the emerging microdialysates, with (13)C NMR analysis, revealed (13)C labeling in glutamine consistent with lactate utilization via the TCA cycle. This suggests that where neurons are too damaged to utilize the lactate produced from glucose by astrocytes, i.e., uncoupling of neuronal and glial metabolism, high extracellular levels of lactate would accumulate, explaining the association between high lactate and poor outcome. Recently, an intravenous exogenous lactate supplementation study in TBI patients revealed evidence for a beneficial effect judged by surrogate endpoints. Here we review the current state of knowledge about glycolysis and lactate in TBI, how it can be measured in patients, and whether it can be modulated to achieve

  16. Clinical practice guidelines for mild traumatic brain injury and persistent symptoms

    PubMed Central

    Marshall, Shawn; Bayley, Mark; McCullagh, Scott; Velikonja, Diana; Berrigan, Lindsay

    2012-01-01

    Abstract Objective To outline new guidelines for the management of mild traumatic brain injury (MTBI) and persistent postconcussive symptoms (PPCS) in order to provide information and direction to physicians managing patients’ recovery from MTBI. Quality of evidence A search for existing clinical practice guidelines addressing MTBI and a systematic review of the literature evaluating treatment of PPCS were conducted. Because little guidance on the management of PPCS was found within the traumatic brain injury field, a second search was completed for clinical practice guidelines and systematic reviews that addressed management of these common symptoms in the general population. Health care professionals representing a range of disciplines from across Canada and abroad were brought together at an expert consensus conference to review the existing guidelines and evidence and to attempt to develop a comprehensive guideline for the management of MTBI and PPCS. Main message A modified Delphi process was used to create 71 recommendations that address the diagnosis and management of MTBI and PPCS. In addition, numerous resources and tools were included in the guideline to aid in the implementation of the recommendations. Conclusion A clinical practice guideline was developed to aid health care professionals in implementing evidence-based, best-practice care for the challenging population of individuals who experience PPCS following MTBI. PMID:22518895

  17. Outcomes of Early Decompressive Craniectomy Versus Conventional Medical Management After Severe Traumatic Brain Injury

    PubMed Central

    Wang, Ren; Li, Mei; Gao, Wen-Wei; Guo, Yan; Chen, Jiong; Tian, Heng-Li

    2015-01-01

    Abstract This meta-analysis examined whether early decompressive craniectomy (DC) can improve control of intracranial pressure (ICP) and mortality in patients with traumatic brain injury (TBI). Medline, Cochrane, EMBASE, and Google Scholar databases were searched until May 14, 2015, using the following terms: traumatic brain injury, refractory intracranial hypertension, high intracranial pressure, craniectomy, standard care, and medical management. Randomized controlled trials in which patients with TBI received DC and non-DC medical treatments were included. Of the 84 articles identified, 8 studies were selected for review, with 3 randomized controlled trials s having a total of 256 patients (123 DCs, 133 non-DCs) included in the meta-analysis. Patients receiving DC had a significantly greater reduction of ICP and shorter hospital stay. They also seemed to have lower odds of death than patients receiving only medical management, but the P value did not reach significance (pooled odds ratio 0.531, 95% confidence interval 0.209–1.350, Z = 1.95, P = 0.183) with respect to the effect on overall mortality; a separate analysis of 3 retrospective studies yielded a similar result. Whereas DC might effectively reduce ICP and shorten hospital stay in patients with TBI, its effect in decreasing mortality has not reached statistical significance. PMID:26512565

  18. Distributions of Magnetic Resonance Diffusion and Spectroscopy Measures with Traumatic Brain Injury

    PubMed Central

    Govind, Varan; Levin, Bonnie; Saigal, Gaurav; Harris, Leo; Sheriff, Sulaiman

    2015-01-01

    Abstract Magnetic resonance spectroscopy (MRS) and diffusion tensor imaging (DTI) studies have demonstrated that measures of altered metabolism and axonal injury can be detected following traumatic brain injury. The aim of this study was to characterize and compare the distributions of altered image parameters obtained by these methods in subjects with a range of injury severity and to examine their relative sensitivity for diagnostic imaging in this group of subjects. DTI and volumetric magnetic resonance spectroscopic imaging data were acquired in 40 subjects that had experienced a closed-head traumatic brain injury, with a median of 36 d post-injury. Voxel-based analyses were performed to examine differences of group mean values relative to normal controls, and to map significant alterations of image parameters in individual subjects. The between-group analysis revealed widespread alteration of tissue metabolites that was most strongly characterized by increased choline throughout the cerebrum and cerebellum, reaching as much as 40% increase from control values for the group with the worse cognitive assessment score. In contrast, the between-group comparison of DTI measures revealed only minor differences; however, the Z-score image analysis of individual subject DTI parameters revealed regions of altered values relative to controls throughout the major white matter tracts, but with considerable heterogeneity between subjects and with a smaller extent than the findings for altered metabolite measures. The findings of this study illustrate the complimentary nature of these neuroimaging methods. PMID:25333480

  19. Sleep Disturbances in Traumatic Brain Injury: A Meta-Analysis

    PubMed Central

    Grima, Natalie; Ponsford, Jennie; Rajaratnam, Shantha M.; Mansfield, Darren; Pase, Matthew P.

    2016-01-01

    Study Objectives: Sleep disturbances are frequently reported following traumatic brain injury (TBI); however, the exact disturbances remain unclear. This meta-analysis aimed to characterize sleep disturbance in community dwelling patients with TBI as compared to controls. Methods: Two investigators independently conducted a systematic search of multiple electronic databases from inception to May 27, 2015. Studies were selected if they compared sleep in community dwelling individuals with TBI relative to a control population without head injury. Data were pooled in meta-analysis with outcomes expressed as the standard mean difference (SMD) and 95% confidence interval (CI). The primary outcomes were derived from polysomnography and secondary outcomes were derived from subjective sleep measures. Results: Sixteen studies were included, combining 637 TBI patients and 567 controls, all of whom were community dwelling. Pooled polysomnography data revealed that TBI patients had poorer sleep efficiency (SMD = −0.47, CI: −0.89, −0.06), shorter total sleep duration (SMD = −0.37, CI: −0.59, −0.16), and greater wake after sleep onset time (SMD = 0.60, CI: 0.33, 0.87). Although sleep architecture was similar between the groups, a trend suggested that TBI patients may spend less time in REM sleep (SMD = −0.22, CI: −0.45, 0.01). Consistent with polysomnographic derangement, TBI patients reported greater subjective sleepiness and poorer perceived sleep quality. Conclusions: The evidence suggests that TBI is associated with widespread objective and subjective sleep deficits. The present results highlight the need for physicians to monitor and address sleep deficits following TBI. Citation: Grima N, Ponsford J, Rajaratnam SM, Mansfield D, Pase MP. Sleep disturbances in traumatic brain injury: a meta-analysis. J Clin Sleep Med 2016;12(3):419–428. PMID:26564384

  20. Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank.

    PubMed

    Bieniek, Kevin F; Ross, Owen A; Cormier, Kerry A; Walton, Ronald L; Soto-Ortolaza, Alexandra; Johnston, Amelia E; DeSaro, Pamela; Boylan, Kevin B; Graff-Radford, Neill R; Wszolek, Zbigniew K; Rademakers, Rosa; Boeve, Bradley F; McKee, Ann C; Dickson, Dennis W

    2015-12-01

    Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder linked to repetitive traumatic brain injury (TBI) and characterized by deposition of hyperphosphorylated tau at the depths of sulci. We sought to determine the presence of CTE pathology in a brain bank for neurodegenerative disorders for individuals with and without a history of contact sports participation. Available medical records of 1721 men were reviewed for evidence of past history of injury or participation in contact sports. Subsequently, cerebral cortical samples were processed for tau immunohistochemistry in cases with a documented history of sports exposure as well as age- and disease-matched men and women without such exposure. For cases with available frozen tissue, genetic analysis was performed for variants in APOE, MAPT, and TMEM106B. Immunohistochemistry revealed 21 of 66 former athletes had cortical tau pathology consistent with CTE. CTE pathology was not detected in 198 individuals without exposure to contact sports, including 33 individuals with documented single-incident TBI sustained from falls, motor vehicle accidents, domestic violence, or assaults. Among those exposed to contact sports, those with CTE pathology did not differ from those without CTE pathology with respect to noted clinicopathologic features. There were no significant differences in genetic variants for those with CTE pathology, but we observed a slight increase in MAPT H1 haplotype, and there tended to be fewer homozygous carriers of the protective TMEM106B rs3173615 minor allele in those with sports exposure and CTE pathology compared to those without CTE pathology. In conclusion, this study has identified a small, yet significant, subset of individuals with neurodegenerative disorders and concomitant CTE pathology. CTE pathology was only detected in individuals with documented participation in contact sports. Exposure to contact sports was the greatest risk factor for CTE pathology. Future

  1. Hyperoxemia and long-term outcome after traumatic brain injury

    PubMed Central

    2013-01-01

    Introduction The relationship between hyperoxemia and outcome in patients with traumatic brain injury (TBI) is controversial. We sought to investigate the independent relationship between hyperoxemia and long-term mortality in patients with moderate-to-severe traumatic brain injury. Methods The Finnish Intensive Care Consortium database was screened for mechanically ventilated patients with a moderate-to-severe TBI. Patients were categorized, according to the highest measured alveolar-arterial O2 gradient or the lowest measured PaO2 value during the first 24 hours of ICU admission, to hypoxemia (<10.0 kPa), normoxemia (10.0 to 13.3 kPa) and hyperoxemia (>13.3 kPa). We adjusted for markers of illness severity to evaluate the independent relationship between hyperoxemia and 6-month mortality. Results A total of 1,116 patients were included in the study, of which 16% (n = 174) were hypoxemic, 51% (n = 567) normoxemic and 33% (n = 375) hyperoxemic. The total 6-month mortality was 39% (n = 435). A significant association between hyperoxemia and a decreased risk of mortality was found in univariate analysis (P = 0.012). However, after adjusting for markers of illness severity in a multivariate logistic regression model hyperoxemia showed no independent relationship with 6-month mortality (hyperoxemia vs. normoxemia OR 0.88, 95% CI 0. 63 to 1.22, P = 0.43; hyperoxemia vs. hypoxemia OR 0.97, 95% CI 0.63 to 1.50, P = 0.90). Conclusion Hyperoxemia in the first 24 hours of ICU admission after a moderate-to-severe TBI is not predictive of 6-month mortality. PMID:23958227

  2. Immune enhancing nutrition in traumatic brain injury - A preliminary study.

    PubMed

    Painter, Thomas J; Rickerds, Jennifer; Alban, Rodrigo F

    2015-09-01

    Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Certain patients appear to benefit when they receive immune enhancing additives, such as glutamine, arginine, and omega-3 fatty acids. We hypothesized that TBI patients given enteral feedings containing these supplements may have improved nutrition measures and infection rates when compared to standard tube feedings. This is a retrospective review of patients from a Level-One trauma center from July 2009 to July 2013. A total of 240 TBI patients received either an immune enhancing nutrition (IEN) formula (n = 126), or a standard formula (SF) (n = 114) based on the attending surgeon's preference. Data collected included demographic information, infection information and outcome measures. Patients were similar in terms of age, ISS, head AIS, and initial prealbumin level. Patients receiving IEN were found to have lower rates of blood stream infections (10.3% vs 19.3%, p < 0.05), whereas pneumonia and UTI rates were similar between groups. In addition, both groups had similar rates of all-cause mortality and hospital length of stay, however IEN patients spent longer in the ICU and on ventilators. In TBI patients receiving IEN, prealbumin levels were higher at the second, third, and fourth week of admission (week 2 - 22.2 vs 17.4, p = 0.006; week 3 - 24.6 vs 20.1, p = 0.04; week 4 - 26.3 vs 22.1, p = 0.19; week 5 - 25.8 vs 20.3, p = 0.21). This study suggests that patients with traumatic brain injury who receive IEN are more likely to have increased prealbumin levels perhaps reflecting improved nutrition throughout their hospital stay and may show some benefit in rates of infections, particularly in bacteremia.

  3. Pharmacologically induced hypothermia attenuates traumatic brain injury in neonatal rats.

    PubMed

    Gu, Xiaohuan; Wei, Zheng Zachory; Espinera, Alyssa; Lee, Jin Hwan; Ji, Xiaoya; Wei, Ling; Dix, Thomas A; Yu, Shan Ping

    2015-05-01

    Neonatal brain trauma is linked to higher risks of mortality and neurological disability. The use of mild to moderate hypothermia has shown promising potential against brain injuries induced by stroke and traumatic brain injury (TBI) in various experimental models and in clinical trials. Conventional methods of physical cooling, however, are difficult to use in acute treatments and in induction of regulated hypothermia. In addition, general anesthesia is usually required to mitigate the negative effects of shivering during physical cooling. Our recent investigations demonstrate the potential therapeutic benefits of pharmacologically induced hypothermia (PIH) using the neurotensin receptor (NTR) agonist HPI201 (formerly known as ABS201) in stroke and TBI models of adult rodents. The present investigation explored the brain protective effects of HPI201 in a P14 rat pediatric model of TBI induced by controlled cortical impact. When administered via intraperitoneal (i.p.) injection, HPI201 induced dose-dependent reduction of body and brain temperature. A 6-h hypothermic treatment, providing an overall 2-3°C reduction of brain and body temperature, showed significant effect of attenuating the contusion volume versus TBI controls. Attenuation occurs whether hypothermia is initiated 15min or 2h after TBI. No shivering response was seen in HPI201-treated animals. HPI201 treatment also reduced TUNEL-positive and TUNEL/NeuN-colabeled cells in the contusion area and peri-injury regions. TBI-induced blood-brain barrier damage was attenuated by HPI201 treatment, evaluated using the Evans Blue assay. HPI201 significantly decreased MMP-9 levels and caspase-3 activation, both of which are pro-apototic, while it increased anti-apoptotic Bcl-2 gene expression in the peri-contusion region. In addition, HPI201 prevented the up-regulation of pro-inflammatory tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6. In sensorimotor activity assessments, rats in the HPI201

  4. Pharmacologically Induced Hypothermia Attenuates Traumatic Brain Injury in Neonatal Rats

    PubMed Central

    Espinera, Alyssa; Lee, Jin Hwan; Ji, Xiaoya; Wei, Ling; Dix, Thomas A.; Yu, Shan Ping

    2015-01-01

    Neonatal brain trauma is linked to higher risks of mortality and neurological disability. The use of mild to moderate hypothermia has shown promising potential against brain injuries induced by stroke and traumatic brain injury (TBI) in various experimental models and in clinical trials. Conventional methods of physical cooling, however, are difficult to use in acute treatments and in induction of regulated hypothermia. In addition, general anesthesia is usually required to mitigate the negative effects of shivering during physical cooling. Our recent investigations demonstrate the potential therapeutic benefits of pharmacologically induced hypothermia (PIH) using the neurotensin receptor (NTR) agonist HPI201 (formerly known as ABS201) in stroke and TBI models of adult rodents. The present investigation explored the brain protective effects of HPI201 in a P14 rat pediatric model of TBI induced by controlled cortical impact. When administered via intraperitoneal (i.p.) injection, HPI201 induced dose-dependent reduction of body and brain temperature. A six-hour hypothermic treatment, providing an overall 2-3°C reduction of brain and body temperature, showed significant effect of attenuating the contusion volume versus TBI controls. Attenuation occurs whether hypothermia is initiated 15 min or 2 hr after TBI. No shivering response was seen in HPI201-treated animals. HPI201 treatment also reduced TUNEL-positive and TUNEL/NeuN-colabeled cells in the contusion area and peri-injury regions. TBI-induced blood brain barrier damage was attenuated by HPI201 treatment, evaluated using the Evans Blue assay. HPI201 significantly decreased MMP-9 levels and Caspase-3 activation, both of which are pro-apototic, while it increased anti-apoptotic Bcl-2 gene expression in the peri-contusion region. In addition, HPI201 prevented the up-regulation of pro-inflammatory tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6. In sensorimotor activity assessments, rats in the

  5. [Optimization of medical-diagnostic process in patients with traumatic brain injury during early rehabilitation].

    PubMed

    Cherednichenko, T V; Popov, A V

    2012-01-01

    The problem of cardiovascular disease and cancer, the effects of traumatic brain injury is now one of the major health and social problems. Every year in Ukraine registered 200 thousand cases of the victims of traumatic brain injury. Of these, 30% of people then have persistent signs of disability that results in a disability, sometimes painful existence the patient and his relatives. Therefore, in order to bring man back into society after a traumatic brain injury, to the rehabilitation phase of treatment, immediately after the stabilization of the patient.

  6. Contribution of Psychological Trauma to Outcomes after Traumatic Brain Injury: Assaults versus Sporting Injuries

    PubMed Central

    Harman-Smith, Yasmin; Bowden, Stephen C.; Rosenfeld, Jeffrey V.; Bigler, Erin D.

    2014-01-01

    Abstract Clinical research into outcomes after traumatic brain injury (TBI) frequently combines injuries that have been sustained through different causes (e.g., car accidents, assaults, and falls), the effect of which is not well understood. This study examined the contribution of injury-related psychological trauma—which is more commonly associated with specific types of injuries—to outcomes after nonpenetrating TBI in order to determine whether it may be having a differential effect in samples containing mixed injuries. Data from three groups that were prospectively recruited for two larger studies were compared: one that sustained a TBI as a result of physical assaults (i.e., psychologically traumatizing) and another as a result of sporting injuries (i.e., nonpsychologically traumatizing), as well as an orthopedic control group (OC). Psychosocial and emotional (postconcussion symptoms, injury-related stress, and depression), cognitive (memory, abstract reasoning, problem solving, and verbal fluency), and functional (general outcome; resumption of home, social, and work roles) outcomes were all assessed. The TBIassault group reported significantly poorer psychosocial and emotional outcomes and higher rates of litigation (criminal rather than civil) than both the TBIsport and OC groups approximately 6 months postinjury, but there were no differences in the cognitive or functional outcomes of the three groups. The findings suggest that the cause of a TBI may assist in explaining some of the differences in outcomes of people who have seemingly comparable injuries. Involvement in litigation and the cause of an injury may also be confounded, which may lead to the erroneous conclusion that litigants have poorer outcomes. PMID:24228916

  7. Relationship between Morphofunctional Changes in Open Traumatic Brain Injury and the Severity of Brain Damage in Rats.

    PubMed

    Shakova, F M; Barskov, I V; Gulyaev, M V; Prokhorenko, S V; Romanova, G A; Grechko, A V

    2016-07-01

    A correlation between the severity of morphofunctional disturbances and the volume of brain tissue injury determined by MRT was demonstrated on the model of open traumatic brain injury in rats. A relationship between the studied parameters (limb placing and beam walking tests and histological changes) and impact force (the height of load fell onto exposed brain surface) was revealed.

  8. Relationship between Morphofunctional Changes in Open Traumatic Brain Injury and the Severity of Brain Damage in Rats.

    PubMed

    Shakova, F M; Barskov, I V; Gulyaev, M V; Prokhorenko, S V; Romanova, G A; Grechko, A V

    2016-07-01

    A correlation between the severity of morphofunctional disturbances and the volume of brain tissue injury determined by MRT was demonstrated on the model of open traumatic brain injury in rats. A relationship between the studied parameters (limb placing and beam walking tests and histological changes) and impact force (the height of load fell onto exposed brain surface) was revealed. PMID:27496035

  9. Return to Work for Persons with Traumatic Brain Injury and Spinal Cord Injury: Three Case Studies.

    ERIC Educational Resources Information Center

    Wehman, Paul; And Others

    1994-01-01

    Supported employment was utilized in the vocational rehabilitation of two people with traumatic brain injury and one with a traumatic spinal cord injury. Supported employment was found to yield real work outcomes, though it required substantial amounts of money to return the three patients to relatively low-paying jobs. Funding issues are…

  10. The role of free radicals in traumatic brain injury.

    PubMed

    O'Connell, Karen M; Littleton-Kearney, Marguerite T

    2013-07-01

    Traumatic brain injury (TBI) is a significant cause of death and disability in both the civilian and the military populations. The primary impact causes initial tissue damage, which initiates biochemical cascades, known as secondary injury, that expand the damage. Free radicals are implicated as major contributors to the secondary injury. Our review of recent rodent and human research reveals the prominent role of the free radicals superoxide anion, nitric oxide, and peroxynitrite in secondary brain injury. Much of our current knowledge is based on rodent studies, and the authors identified a gap in the translation of findings from rodent to human TBI. Rodent models are an effective method for elucidating specific mechanisms of free radical-induced injury at the cellular level in a well-controlled environment. However, human TBI does not occur in a vacuum, and variables controlled in the laboratory may affect the injury progression. Additionally, multiple experimental TBI models are accepted in rodent research, and no one model fully reproduces the heterogeneous injury seen in humans. Free radical levels are measured indirectly in human studies based on assumptions from the findings from rodent studies that use direct free radical measurements. Further study in humans should be directed toward large samples to validate the findings in rodent studies. Data obtained from these studies may lead to more targeted treatment to interrupt the secondary injury cascades.

  11. Diagnosis, prognosis, and clinical management of mild traumatic brain injury.

    PubMed

    Levin, Harvey S; Diaz-Arrastia, Ramon R

    2015-05-01

    Concussion and mild traumatic brain injury (TBI) are interchangeable terms to describe a common disorder with substantial effects on public health. Advances in brain imaging, non-imaging biomarkers, and neuropathology during the past 15 years have required researchers, clinicians, and policy makers to revise their views about mild TBI as a fully reversible insult that can be repeated without consequences. These advances have led to guidelines on management of mild TBI in civilians, military personnel, and athletes, but their widespread dissemination to clinical management in emergency departments and community-based health care is still needed. The absence of unity on the definition of mild TBI, the scarcity of prospective data concerning the long-term effects of repeated mild TBI and subconcussive impacts, and the need to further develop evidence-based interventions to mitigate the long-term sequelae are areas for future research that will improve outcomes, reduce morbidity and costs, and alleviate delayed consequences that have only recently come to light. PMID:25801547

  12. Acetazolamide Mitigates Astrocyte Cellular Edema Following Mild Traumatic Brain Injury

    NASA Astrophysics Data System (ADS)

    Sturdivant, Nasya M.; Smith, Sean G.; Ali, Syed F.; Wolchok, Jeffrey C.; Balachandran, Kartik

    2016-09-01

    Non-penetrating or mild traumatic brain injury (mTBI) is commonly experienced in accidents, the battlefield and in full-contact sports. Astrocyte cellular edema is one of the major factors that leads to high morbidity post-mTBI. Various studies have reported an upregulation of aquaporin-4 (AQP4), a water channel protein, following brain injury. AZA is an antiepileptic drug that has been shown to inhibit AQP4 expression and in this study we investigate the drug as a therapeutic to mitigate the extent of mTBI induced cellular edema. We hypothesized that mTBI-mediated astrocyte dysfunction, initiated by increased intracellular volume, could be reduced when treated with AZA. We tested our hypothesis in a three-dimensional in vitro astrocyte model of mTBI. Samples were subject to no stretch (control) or one high-speed stretch (mTBI) injury. AQP4 expression was significantly increased 24 hours after mTBI. mTBI resulted in a significant increase in the cell swelling within 30 min of mTBI, which was significantly reduced in the presence of AZA. Cell death and expression of S100B was significantly reduced when AZA was added shortly before mTBI stretch. Overall, our data point to occurrence of astrocyte swelling immediately following mTBI, and AZA as a promising treatment to mitigate downstream cellular mortality.

  13. Fluid-percussion–induced traumatic brain injury model in rats

    PubMed Central

    Kabadi, Shruti V.; Hilton, Genell D.; Stoica, Bogdan A.; Zapple, David N.; Faden, Alan I.

    2013-01-01

    Traumatic brain injury (TBI) is a major cause of mortality and morbidity. Various attempts have been made to replicate clinical TBI using animal models. The fluid-percussion model (FP) is one of the oldest and most commonly used models of experimentally induced TBI. Both central (CFP) and lateral (LFP) variations of the model have been used. Developed initially for use in larger species, the standard FP device was adapted more than 20 years ago to induce consistent degrees of brain injury in rodents. Recently, we developed a microprocessor-controlled, pneumatically driven instrument, micro-FP (MFP), to address operational concerns associated with the use of the standard FP device in rodents. We have characterized the MFP model with regard to injury severity according to behavioral and histological outcomes. In this protocol, we review the FP models and detail surgical procedures for LFP. The surgery involves tracheal intubation, craniotomy and fixation of Luer fittings, and induction of injury. The surgical procedure can be performed within 45–50 min. PMID:20725070

  14. Acetazolamide Mitigates Astrocyte Cellular Edema Following Mild Traumatic Brain Injury

    PubMed Central

    Sturdivant, Nasya M.; Smith, Sean G.; Ali, Syed F.; Wolchok, Jeffrey C.; Balachandran, Kartik

    2016-01-01

    Non-penetrating or mild traumatic brain injury (mTBI) is commonly experienced in accidents, the battlefield and in full-contact sports. Astrocyte cellular edema is one of the major factors that leads to high morbidity post-mTBI. Various studies have reported an upregulation of aquaporin-4 (AQP4), a water channel protein, following brain injury. AZA is an antiepileptic drug that has been shown to inhibit AQP4 expression and in this study we investigate the drug as a therapeutic to mitigate the extent of mTBI induced cellular edema. We hypothesized that mTBI-mediated astrocyte dysfunction, initiated by increased intracellular volume, could be reduced when treated with AZA. We tested our hypothesis in a three-dimensional in vitro astrocyte model of mTBI. Samples were subject to no stretch (control) or one high-speed stretch (mTBI) injury. AQP4 expression was significantly increased 24 hours after mTBI. mTBI resulted in a significant increase in the cell swelling within 30 min of mTBI, which was significantly reduced in the presence of AZA. Cell death and expression of S100B was significantly reduced when AZA was added shortly before mTBI stretch. Overall, our data point to occurrence of astrocyte swelling immediately following mTBI, and AZA as a promising treatment to mitigate downstream cellular mortality. PMID:27623738

  15. A better mild traumatic brain injury model in the rat.

    PubMed

    Takeuchi, Satoru; Nawashiro, Hiroshi; Sato, Shunichi; Kawauchi, Satoko; Nagatani, Kimihiro; Kobayashi, Hiroaki; Otani, Naoki; Osada, Hideo; Wada, Kojiro; Shima, Katsuji

    2013-01-01

    The primary pathology associated with mild -traumatic brain injury (TBI) is selective axonal injury, which may characterize the vast majority of blast-induced TBIs. Axonal injuries in cases of mild TBI have been considered to be the main factors responsible for the long-lasting memory or attentional impairment in affected subjects. Among these axonal injuries, recent attention has been focused on the cingulum bundle (CB). Furthermore, recent studies with diffusion tensor MR imaging have shown the presence of injuries of the CB in cases of mild TBI in humans. This study aimed to provide a better laboratory model of mild TBI.Sprague-Dawley rats were subjected to mild TBI using laser-induced shock waves (LISW) (sham, 0.5 J/cm(2), or 1.0 J/cm(2); n = 4 per group). Bodian-stained brain sections 14 days after LISW at 0.5 J/cm(2) or 1.0 J/cm(2) showed a decrease in the CB axonal density compared with the sham group, whereas there were no differences in the axonal density of the corpus callosum.The present study shows that this model is capable of reproducing the histological changes associated with mild TBI. PMID:23564112

  16. A multidimensional approach to apathy after traumatic brain injury.

    PubMed

    Arnould, Annabelle; Rochat, Lucien; Azouvi, Philippe; Van der Linden, Martial

    2013-09-01

    Apathy is commonly described following traumatic brain injury (TBI) and is associated with serious consequences, notably for patients' participation in rehabilitation, family life and later social reintegration. There is strong evidence in the literature of the multidimensional nature of apathy (behavioural, cognitive and emotional), but the processes underlying each dimension are still unclear. The purpose of this article is first, to provide a critical review of the current definitions and instruments used to measure apathy in neurological and psychiatric disorders, and second, to review the prevalence, characteristics, neuroanatomical correlates, relationships with other neurobehavioural disorders and mechanisms of apathy in the TBI population. In this context, we propose a new multidimensional framework that takes into account the various mechanisms at play in the facets of apathy, including not only cognitive factors, especially executive, but also affective factors (e.g., negative mood), motivational variables (e.g., anticipatory pleasure) and aspects related to personal identity (e.g., self-esteem). Future investigations that consider these various factors will help improve the understanding of apathy. This theoretical framework opens up relevant prospects for better clinical assessment and rehabilitation of these frequently described motivational disorders in patients with brain injury. PMID:23921453

  17. Past, Present, and Future of Traumatic Brain Injury Research.

    PubMed

    Hawryluk, Gregory W J; Bullock, M Ross

    2016-10-01

    Traumatic brain injury (TBI) is the greatest cause of death and severe disability in young adults; its incidence is increasing in the elderly and in the developing world. Outcome from severe TBI has improved dramatically as a result of advancements in trauma systems and supportive critical care, however we remain without a therapeutic which acts directly to attenuate brain injury. Recognition of secondary injury and its molecular mediators has raised hopes for such targeted treatments. Unfortunately, over 30 late-phase clinical trials investigating promising agents have failed to translate a therapeutic for clinical use. Numerous explanations for this failure have been postulated and are reviewed here. With this historical context we review ongoing research and anticipated future trends which are armed with lessons from past trials, new scientific advances, as well as improved research infrastructure and funding. There is great hope that these new efforts will finally lead to an effective therapeutic for TBI as well as better clinical management strategies. PMID:27637391

  18. Acetazolamide Mitigates Astrocyte Cellular Edema Following Mild Traumatic Brain Injury.

    PubMed

    Sturdivant, Nasya M; Smith, Sean G; Ali, Syed F; Wolchok, Jeffrey C; Balachandran, Kartik

    2016-01-01

    Non-penetrating or mild traumatic brain injury (mTBI) is commonly experienced in accidents, the battlefield and in full-contact sports. Astrocyte cellular edema is one of the major factors that leads to high morbidity post-mTBI. Various studies have reported an upregulation of aquaporin-4 (AQP4), a water channel protein, following brain injury. AZA is an antiepileptic drug that has been shown to inhibit AQP4 expression and in this study we investigate the drug as a therapeutic to mitigate the extent of mTBI induced cellular edema. We hypothesized that mTBI-mediated astrocyte dysfunction, initiated by increased intracellular volume, could be reduced when treated with AZA. We tested our hypothesis in a three-dimensional in vitro astrocyte model of mTBI. Samples were subject to no stretch (control) or one high-speed stretch (mTBI) injury. AQP4 expression was significantly increased 24 hours after mTBI. mTBI resulted in a significant increase in the cell swelling within 30 min of mTBI, which was significantly reduced in the presence of AZA. Cell death and expression of S100B was significantly reduced when AZA was added shortly before mTBI stretch. Overall, our data point to occurrence of astrocyte swelling immediately following mTBI, and AZA as a promising treatment to mitigate downstream cellular mortality. PMID:27623738

  19. Neuroprotective effects of geranylgeranylacetone in experimental traumatic brain injury.

    PubMed

    Zhao, Zaorui; Faden, Alan I; Loane, David J; Lipinski, Marta M; Sabirzhanov, Boris; Stoica, Bogdan A

    2013-12-01

    Geranylgeranylacetone (GGA) is an inducer of heat-shock protein 70 (HSP70) that has been used clinically for many years as an antiulcer treatment. It is centrally active after oral administration and is neuroprotective in experimental brain ischemia/stroke models. We examined the effects of single oral GGA before treatment (800 mg/kg, 48 hours before trauma) or after treatment (800 mg/kg, 3 hours after trauma) on long-term functional recovery and histologic outcomes after moderate-level controlled cortical impact, an experimental traumatic brain injury (TBI) model in mice. The GGA pretreatment increased the number of HSP70(+) cells and attenuated posttraumatic α-fodrin cleavage, a marker of apoptotic cell death. It also improved sensorimotor performance on a beam walk task; enhanced recovery of cognitive/affective function in the Morris water maze, novel object recognition, and tail-suspension tests; and improved outcomes using a composite neuroscore. Furthermore, GGA pretreatment reduced the lesion size and neuronal loss in the hippocampus, cortex, and thalamus, and decreased microglial activation in the cortex when compared with vehicle-treated TBI controls. Notably, GGA was also effective in a posttreatment paradigm, showing significant improvements in sensorimotor function, and reducing cortical neuronal loss. Given these neuroprotective actions and considering its longstanding clinical use, GGA should be considered for the clinical treatment of TBI. PMID:23942364

  20. The experience of traumatic brain injury in Botswana.

    PubMed

    Mbakile-Mahlanza, Lingani; Manderson, Lenore; Ponsford, Jennie

    2015-01-01

    Whilst the consequences of traumatic brain injury (TBI) are understood in Western countries, it is not known how cultural background and beliefs affect response and outcome following TBI in low and middle income countries. This study aimed to explore the experiences of TBI in Botswana. Participants included 21 individuals with moderate to severe TBI (68% males, mean age 35.2 years), 18 caregivers and 25 healthcare workers. Qualitative semi-structured interviews were transcribed, translated and thematically coded. Thematic analysis indicated several themes: Injury-related changes, attributions and beliefs about the cause of the injury, family reactions, attitudes, and resources. Participants described the common injury-related effects of TBI. Many participants attributed their injury to supernatural causes. Immediate family members of participants with TBI expressed a sense of love and devotion towards the injured person. Communication was characterised by inadequate information given to those injured and their caregivers. Provision of care was impeded by insufficient staff, limited supplies and lack of training of nurses. The current healthcare system would therefore appear to be ill-equipped to meet the needs of TBI survivors in Botswana. This study will improve understanding of cultural responses and approaches to brain injuries in Botswana which may, in turn, inform improved practice. PMID:25558888

  1. Experimental modeling of explosive blast-related traumatic brain injuries.

    PubMed

    Alley, Matthew D; Schimizze, Benjamin R; Son, Steven F

    2011-01-01

    This study aims to characterize the interaction of explosive blast waves through simulated anatomical systems. We have developed physical models and a systematic approach for testing traumatic brain injury (TBI) mechanisms and occurrences. A simplified series of models consisting of spherical poly(methyl methacrylate) (PMMA) shells housing synthetic gelatins as brain simulants have been utilized. A series of experiments was conducted to compare the sensitivity of the system response to mechanical properties of the simulants under high strain-rate explosive blasts. Small explosive charges were directed at the models to produce a realistic blast wave in a scaled laboratory setting. Blast profiles were measured and analyzed to compare system response severity. High-speed shadowgraph imaging captured blast wave interaction with the head model while particle tracking captured internal response for displacement and strain correlation. The results suggest amplification of shock waves inside the head near material interfaces due to impedance mismatches. In addition, significant relative displacement was observed between the interacting materials suggesting large strain values of nearly 5%. Further quantitative results were obtained through shadowgraph imaging of the blasts confirming a separation of time scales between blast interaction and bulk movement. These results lead to a conclusion that primary blast effects may potentially contribute significantly to the occurrence of military associated TBI. PMID:20580931

  2. Cognitive and psychopathological sequelae of pediatric traumatic brain injury.

    PubMed

    Beauchamp, M H; Anderson, V

    2013-01-01

    Childhood traumatic brain injury (TBI) is a frequent cause of acquired disability in childhood and can have a serious impact on development across the lifespan. The consequences of early TBI vary according to injury severity, with severe injuries usually resulting in more serious physical, cognitive and behavioral sequelae. Both clinical and research reports document residual deficits in a range of skills, including intellectual function, attention, memory, learning, and executive function. In addition, recent investigations suggest that early brain injury also affects psychological and social development and that problems in these domains may increase in the long term postinjury. Together, these deficits affect children's ability to function effectively at school, in the home, and in their social environment, resulting in impaired acquisition of knowledge, psychological and social problems, and overall reduced quality of life. Ultimately, recovery from childhood TBI depends on a range of complex biological, developmental, and psychosocial factors making prognosis difficult to predict. This chapter will detail the cognitive (intellectual, attentional, mnesic, executive, educational, and vocational) and psychopathological (behavioral, adaptive, psychological, social) sequelae of childhood TBI with a particular focus on postinjury recovery patterns in the acute, short-, and long-term phases, as well as into adulthood. PMID:23622301

  3. Verbal learning patterns in moderate and severe traumatic brain injury.

    PubMed

    Millis, S R; Ricker, J H

    1994-08-01

    Previous studies that have examined performances on the California Verbal Learning Test (CVLT) among individuals with traumatic brain injury (TBI) have found differing levels of performance. Differential patterns of performance, however, have only been inferred. The present investigation sought to determine empirically if differential patterns of performance could be discerned in a TBI sample of 65 subjects with CVLT variables. The CVLT variables were selected based on the instrument's factor structure. Cluster analysis yielded four distinct subtypes of brain-injured individuals. The Active subtype demonstrated impaired unassisted retrieval, but used active encoding strategies and showed relatively intact ability to store novel information. The Disorganized subtype demonstrated an inconsistent, haphazard learning style along with deficits in encoding. The Passive subtype was marked by an overreliance on a serial clustering strategy as well as impaired encoding and/or consolidation. The Deficient subtype was the most impaired of all groups, exhibiting a slowed rate of acquisition, passive learning style, and significant impairment in encoding. Implications for rehabilitation are discussed.

  4. Blast-related mild traumatic brain injury: mechanisms of injury and impact on clinical care.

    PubMed

    Elder, Gregory A; Cristian, Adrian

    2009-04-01

    Mild traumatic brain injury has been called the signature injury of the wars in Iraq and Afghanistan. In both theaters of operation, traumatic brain injury has been a significant cause of mortality and morbidity, with blast-related injury the most common cause. Improvised explosive devices have been the major cause of blast injuries. It is estimated that 10% to 20% of veterans returning from these operations have suffered a traumatic brain injury, and there is concern that blast-related injury may produce adverse long-term health affects and affect the resilience and in-theater performance of troops. Blast-related injury occurs through several mechanisms related to the nature of the blast overpressure wave itself as well as secondary and tertiary injuries. Animal studies clearly show that blast overpressure waves are transmitted to the brain and can cause changes that neuropathologically are most similar to diffuse axonal injury. One striking feature of the mild traumatic brain injury cases being seen in veterans of the wars in Iraq and Afghanistan is the high association of mild traumatic brain injury with posttraumatic stress disorder. The overlap in symptoms between the disorders has made distinguishing them clinically challenging. The high rates of mild traumatic brain injury and posttraumatic stress disorder in the current operations are of significant concern for the long-term health of US veterans with associated economic implications. PMID:19306373

  5. Clinical review: Brain-body temperature differences in adults with severe traumatic brain injury.

    PubMed

    Childs, Charmaine; Lunn, Kueh Wern

    2013-04-22

    Surrogate or 'proxy' measures of brain temperature are used in the routine management of patients with brain damage. The prevailing view is that the brain is 'hotter' than the body. The polarity and magnitude of temperature differences between brain and body, however, remains unclear after severe traumatic brain injury (TBI). The focus of this systematic review is on the adult patient admitted to intensive/neurocritical care with a diagnosis of severe TBI (Glasgow Coma Scale score of less than 8). The review considered studies that measured brain temperature and core body temperature. Articles published in English from the years 1980 to 2012 were searched in databases, CINAHL, PubMed, Scopus, Web of Science, Science Direct, Ovid SP, Mednar and ProQuest Dissertations & Theses Database. For the review, publications of randomised controlled trials, non-randomised controlled trials, before and after studies, cohort studies, case-control studies and descriptive studies were considered for inclusion. Of 2,391 records identified via the search strategies, 37 were retrieved for detailed examination (including two via hand searching). Fifteen were reviewed and assessed for methodological quality. Eleven studies were included in the systematic review providing 15 brain-core body temperature comparisons. The direction of mean brain-body temperature differences was positive (brain higher than body temperature) and negative (brain lower than body temperature). Hypothermia is associated with large brain-body temperature differences. Brain temperature cannot be predicted reliably from core body temperature. Concurrent monitoring of brain and body temperature is recommended in patients where risk of temperature-related neuronal damage is a cause for clinical concern and when deliberate induction of below-normal body temperature is instituted.

  6. Alterations in Cholinergic Pathways and Therapeutic Strategies Targeting Cholinergic System after Traumatic Brain Injury

    PubMed Central

    Shin, Samuel S.

    2015-01-01

    Abstract Traumatic brain injury (TBI) results in varying degrees of disability in a significant number of persons annually. The mechanisms of cognitive dysfunction after TBI have been explored in both animal models and human clinical studies for decades. Dopaminergic, serotonergic, and noradrenergic dysfunction has been described in many previous reports. In addition, cholinergic dysfunction has also been a familiar topic among TBI researchers for many years. Although pharmacological agents that modulate cholinergic neurotransmission have been used with varying degrees of success in previous studies, improving their function and maximizing cognitive recovery is an ongoing process. In this article, we review the previous findings on the biological mechanism of cholinergic dysfunction after TBI. In addition, we describe studies that use both older agents and newly developed agents as candidates for targeting cholinergic neurotransmission in future studies. PMID:25646580

  7. Chronic Decrease in Wakefulness and Disruption of Sleep-Wake Behavior after Experimental Traumatic Brain Injury

    PubMed Central

    Skopin, Mark D.; Kabadi, Shruti V.; Viechweg, Shaun S.; Mong, Jessica A.

    2015-01-01

    Abstract Traumatic brain injury (TBI) can cause sleep-wake disturbances and excessive daytime sleepiness. The pathobiology of sleep disorders in TBI, however, is not well understood, and animal models have been underused in studying such changes and potential underlying mechanisms. We used the rat lateral fluid percussion (LFP) model to analyze sleep-wake patterns as a function of time after injury. Rapid-eye movement (REM) sleep, non-REM (NREM) sleep, and wake bouts during light and dark phases were measured with electroencephalography and electromyography at an early as well as chronic time points after LFP. Moderate TBI caused disturbances in the ability to maintain consolidated wake bouts during the active phase and chronic loss of wakefulness. Further, TBI resulted in cognitive impairments and depressive-like symptoms, and reduced the number of orexin-A-positive neurons in the lateral hypothalamus. PMID:25242371

  8. Dementia resulting from traumatic brain injury: what is the pathology?

    PubMed

    Shively, Sharon; Scher, Ann I; Perl, Daniel P; Diaz-Arrastia, Ramon

    2012-10-01

    Traumatic brain injury (TBI) is among the earliest illnesses described in human history and remains a major source of morbidity and mortality in the modern era. It is estimated that 2% of the US population lives with long-term disabilities due to a prior TBI, and incidence and prevalence rates are even higher in developing countries. One of the most feared long-term consequences of TBIs is dementia, as multiple epidemiologic studies show that experiencing a TBI in early or midlife is associated with an increased risk of dementia in late life. The best data indicate that moderate and severe TBIs increase risk of dementia between 2- and 4-fold. It is less clear whether mild TBIs such as brief concussions result in increased dementia risk, in part because mild head injuries are often not well documented and retrospective studies have recall bias. However, it has been observed for many years that multiple mild TBIs as experienced by professional boxers are associated with a high risk of chronic traumatic encephalopathy (CTE), a type of dementia with distinctive clinical and pathologic features. The recent recognition that CTE is common in retired professional football and hockey players has rekindled interest in this condition, as has the recognition that military personnel also experience high rates of mild TBIs and may have a similar syndrome. It is presently unknown whether dementia in TBI survivors is pathophysiologically similar to Alzheimer disease, CTE, or some other entity. Such information is critical for developing preventive and treatment strategies for a common cause of acquired dementia. Herein, we will review the epidemiologic data linking TBI and dementia, existing clinical and pathologic data, and will identify areas where future research is needed.

  9. Neuropsychiatric disturbances and hypopituitarism after traumatic brain injury in an elderly man.

    PubMed

    Chang, Yi-Cheng; Tsai, Jui-Chang; Tseng, Fen-Yu

    2006-02-01

    Neuropsychiatric or cognitive disturbances are common complications after traumatic brain injury. They are commonly regarded as irreversible sequelae of organic brain injuries. We report a case of hypopituitarism in a 77-year-old man who presented with long-term neuropsychiatric disturbances, including cognitive impairment, disturbed sleep patterns, personality change, loss of affect, and visual and auditory hallucinations after a traumatic subdural hemorrhage. The treatment response to hormone replacement therapy was nearly complete. Hypopituitarism is rarely considered in patients who sustain traumatic brain injury and the neuropsychiatric manifestations of posttraumatic hypopituitarism have rarely been reported. This case highlights the importance of hypopituitarism as a potential reversible cause of neuropsychiatric disturbances after traumatic brain injury.

  10. Translational Research for Blast-Induced Traumatic Brain Injury: Injury Mechanism to Development of Medical Instruments

    NASA Astrophysics Data System (ADS)

    Nakagawa, A.; Ohtani, K.; Arafune, T.; Washio, T.; Iwasaki, M.; Endo, T.; Ogawa, Y.; Kumabe, T.; Takayama, K.; Tominaga, T.

    1. Investigation of shock wave-induced phenomenon: blast-induced traumatic brain injury Blast wave (BW) is generated by explosion and is comprised of lead shock wave (SE) followed by subsequent supersonic flow.

  11. Tensor-Based Morphometry Reveals Volumetric Deficits in Moderate=Severe Pediatric Traumatic Brain Injury

    PubMed Central

    Hua, Xue; Villalon-Reina, Julio; Moran, Lisa M.; Kernan, Claudia; Babikian, Talin; Mink, Richard; Babbitt, Christopher; Johnson, Jeffrey; Giza, Christopher C.; Thompson, Paul M.; Asarnow, Robert F.

    2016-01-01

    Abstract Traumatic brain injury (TBI) can cause widespread and prolonged brain degeneration. TBI can affect cognitive function and brain integrity for many years after injury, often with lasting effects in children, whose brains are still immature. Although TBI varies in how it affects different individuals, image analysis methods such as tensor-based morphometry (TBM) can reveal common areas of brain atrophy on magnetic resonance imaging (MRI), secondary effects of the initial injury, which will differ between subjects. Here we studied 36 pediatric moderate to severe TBI (msTBI) participants in the post-acute phase (1–6 months post-injury) and 18 msTBI participants who returned for their chronic assessment, along with well-matched controls at both time-points. Participants completed a battery of cognitive tests that we used to create a global cognitive performance score. Using TBM, we created three-dimensional (3D) maps of individual and group differences in regional brain volumes. At both the post-acute and chronic time-points, the greatest group differences were expansion of the lateral ventricles and reduction of the lingual gyrus in the TBI group. We found a number of smaller clusters of volume reduction in the cingulate gyrus, thalamus, and fusiform gyrus, and throughout the frontal, temporal, and parietal cortices. Additionally, we found extensive associations between our cognitive performance measure and regional brain volume. Our results indicate a pattern of atrophy still detectable 1-year post-injury, which may partially underlie the cognitive deficits frequently found in TBI. PMID:26393494

  12. Charting a course for erythropoietin in traumatic brain injury

    PubMed Central

    Maiese, Kenneth

    2016-01-01

    Traumatic brain injury (TBI) is a severe public health problem that impacts more than four million individuals in the United States alone and is increasing in incidence on a global scale. Importantly, TBI can result in acute as well as chronic impairments for the nervous system leaving individuals with chronic disability and in instances of severe trauma, death becomes the ultimate outcome. In light of the significant negative health consequences of TBI, multiple therapeutic strategies are under investigation, but those focusing upon the cytokine and growth factor erythropoietin (EPO) have generated a great degree of enthusiasm. EPO can control cell death pathways tied to apoptosis and autophagy as well oversees processes that affect cellular longevity and aging. In vitro studies and experimental animal models of TBI have shown that EPO can restore axonal integrity, promote cellular proliferation, reduce brain edema, and preserve cellular energy homeostasis and mitochondrial function. Clinical studies for neurodegenerative disorders that involve loss of cognition or developmental brain injury support a positive role for EPO to prevent or reduce injury in the nervous system. However, recent clinical trials with EPO and TBI have not produced such clear conclusions. Further clinical studies are warranted to address the potential efficacy of EPO during TBI, the concerns with the onset, extent, and duration of EPO therapeutic strategies, and to focus upon the specific downstream pathways controlled by EPO such as protein kinase B (Akt), mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), sirtuins, wingless pathways, and forkhead transcription factors for improved precision against the detrimental effects of TBI. PMID:27081573

  13. Systems Biology, Neuroimaging, Neuropsychology, Neuroconnectivity and Traumatic Brain Injury

    PubMed Central

    Bigler, Erin D.

    2016-01-01

    The patient who sustains a traumatic brain injury (TBI) typically undergoes neuroimaging studies, usually in the form of computed tomography (CT) and magnetic resonance imaging (MRI). In most cases the neuroimaging findings are clinically assessed with descriptive statements that provide qualitative information about the presence/absence of visually identifiable abnormalities; though little if any of the potential information in a scan is analyzed in any quantitative manner, except in research settings. Fortunately, major advances have been made, especially during the last decade, in regards to image quantification techniques, especially those that involve automated image analysis methods. This review argues that a systems biology approach to understanding quantitative neuroimaging findings in TBI provides an appropriate framework for better utilizing the information derived from quantitative neuroimaging and its relation with neuropsychological outcome. Different image analysis methods are reviewed in an attempt to integrate quantitative neuroimaging methods with neuropsychological outcome measures and to illustrate how different neuroimaging techniques tap different aspects of TBI-related neuropathology. Likewise, how different neuropathologies may relate to neuropsychological outcome is explored by examining how damage influences brain connectivity and neural networks. Emphasis is placed on the dynamic changes that occur following TBI and how best to capture those pathologies via different neuroimaging methods. However, traditional clinical neuropsychological techniques are not well suited for interpretation based on contemporary and advanced neuroimaging methods and network analyses. Significant improvements need to be made in the cognitive and behavioral assessment of the brain injured individual to better interface with advances in neuroimaging-based network analyses. By viewing both neuroimaging and neuropsychological processes within a systems biology

  14. Pathophysiology of microwave-induced traumatic brain injury

    PubMed Central

    IGARASHI, YUTAKA; MATSUDA, YOKO; FUSE, AKIRA; ISHIWATA, TOSHIYUKI; NAITO, ZENYA; YOKOTA, HIROYUKI

    2015-01-01

    Microwave technology has been widely used in numerous applications; however, excessive microwave exposure causes adverse effects, particularly in the brain. The present study aimed to evaluate the change in the number of neural cells and presence of apoptotic cells in rats for one month after exposure to excessive microwave radiation. The rats were exposed to 3.0 kW of microwaves for 0.1 sec and were sacrificed after 24 h (n=3), or 3 (n=3), 7 (n=3), 14 (n=3) or 28 days (n=4) of exposure. The neural cells were counted in the motor cortex and hippocampus [cornu ammonis 1 (CA1) and CA2] and the percentage of positive cells stained with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) were also measured, which detected apoptotic cell death in the choroid plexus in the lateral ventricle, motor cortex and hippocampus. In the CA1, the number of neural cells decreased significantly by day 28 compared with that in the control (60.7 vs. 50.6, P=0.0358), but did not decrease before day 28. There were no significant differences on any day in the CA2 and the motor cortex. The number of cells showed a significant increase on day 7 compared to the control in the choroid plexus (2.1±1.1 vs. 21.8±19.1%, P=0.0318). There were no significant differences from the controls in the percentage of TUNEL-positive cells in the motor cortex and hippocampus. The effects of microwave exposure on the brain remain unclear; however, microwave-induced neurotrauma shows the same pathological changes as blast traumatic brain injury. PMID:26171150

  15. Systems Biology, Neuroimaging, Neuropsychology, Neuroconnectivity and Traumatic Brain Injury.

    PubMed

    Bigler, Erin D

    2016-01-01

    The patient who sustains a traumatic brain injury (TBI) typically undergoes neuroimaging studies, usually in the form of computed tomography (CT) and magnetic resonance imaging (MRI). In most cases the neuroimaging findings are clinically assessed with descriptive statements that provide qualitative information about the presence/absence of visually identifiable abnormalities; though little if any of the potential information in a scan is analyzed in any quantitative manner, except in research settings. Fortunately, major advances have been made, especially during the last decade, in regards to image quantification techniques, especially those that involve automated image analysis methods. This review argues that a systems biology approach to understanding quantitative neuroimaging findings in TBI provides an appropriate framework for better utilizing the information derived from quantitative neuroimaging and its relation with neuropsychological outcome. Different image analysis methods are reviewed in an attempt to integrate quantitative neuroimaging methods with neuropsychological outcome measures and to illustrate how different neuroimaging techniques tap different aspects of TBI-related neuropathology. Likewise, how different neuropathologies may relate to neuropsychological outcome is explored by examining how damage influences brain connectivity and neural networks. Emphasis is placed on the dynamic changes that occur following TBI and how best to capture those pathologies via different neuroimaging methods. However, traditional clinical neuropsychological techniques are not well suited for interpretation based on contemporary and advanced neuroimaging methods and network analyses. Significant improvements need to be made in the cognitive and behavioral assessment of the brain injured individual to better interface with advances in neuroimaging-based network analyses. By viewing both neuroimaging and neuropsychological processes within a systems biology

  16. Systems Biology, Neuroimaging, Neuropsychology, Neuroconnectivity and Traumatic Brain Injury.

    PubMed

    Bigler, Erin D

    2016-01-01

    The patient who sustains a traumatic brain injury (TBI) typically undergoes neuroimaging studies, usually in the form of computed tomography (CT) and magnetic resonance imaging (MRI). In most cases the neuroimaging findings are clinically assessed with descriptive statements that provide qualitative information about the presence/absence of visually identifiable abnormalities; though little if any of the potential information in a scan is analyzed in any quantitative manner, except in research settings. Fortunately, major advances have been made, especially during the last decade, in regards to image quantification techniques, especially those that involve automated image analysis methods. This review argues that a systems biology approach to understanding quantitative neuroimaging findings in TBI provides an appropriate framework for better utilizing the information derived from quantitative neuroimaging and its relation with neuropsychological outcome. Different image analysis methods are reviewed in an attempt to integrate quantitative neuroimaging methods with neuropsychological outcome measures and to illustrate how different neuroimaging techniques tap different aspects of TBI-related neuropathology. Likewise, how different neuropathologies may relate to neuropsychological outcome is explored by examining how damage influences brain connectivity and neural networks. Emphasis is placed on the dynamic changes that occur following TBI and how best to capture those pathologies via different neuroimaging methods. However, traditional clinical neuropsychological techniques are not well suited for interpretation based on contemporary and advanced neuroimaging methods and network analyses. Significant improvements need to be made in the cognitive and behavioral assessment of the brain injured individual to better interface with advances in neuroimaging-based network analyses. By viewing both neuroimaging and neuropsychological processes within a systems biology

  17. A Wireless Intracranial Brain Deformation Sensing System for Blast-Induced Traumatic Brain Injury

    PubMed Central

    Song, S.; Race, N. S.; Kim, A.; Zhang, T.; Shi, R.; Ziaie, B.

    2015-01-01

    Blast-induced traumatic brain injury (bTBI) has been linked to a multitude of delayed-onset neurodegenerative and neuropsychiatric disorders, but complete understanding of their pathogenesis remains elusive. To develop mechanistic relationships between bTBI and post-blast neurological sequelae, it is imperative to characterize the initiating traumatic mechanical events leading to eventual alterations of cell, tissue, and organ structure and function. This paper presents a wireless sensing system capable of monitoring the intracranial brain deformation in real-time during the event of a bTBI. The system consists of an implantable soft magnet and an external head-mounted magnetic sensor that is able to measure the field in three dimensions. The change in the relative position of the soft magnet WITH respect to the external sensor as the result of the blast wave induces changes in the magnetic field. The magnetic field data in turn is used to extract the temporal and spatial motion of the brain under the blast wave in real-time. The system has temporal and spatial resolutions of 5 μs and 10 μm. Following the characterization and validation of the sensor system, we measured brain deformations in a live rodent during a bTBI. PMID:26586273

  18. Diffuse traumatic brain injury induces prolonged immune dysregulation and potentiates hyperalgesia following a peripheral immune challenge

    PubMed Central

    Rowe, Rachel K; Ellis, Gavin I; Harrison, Jordan L; Bachstetter, Adam D; Corder, Gregory F; Van Eldik, Linda J; Taylor, Bradley K; Marti, Francesc

    2016-01-01

    Background Nociceptive and neuropathic pain occurs as part of the disease process after traumatic brain injury (TBI) in humans. Central and peripheral inflammation, a major secondary injury process initiated by the traumatic brain injury event, has been implicated in the potentiation of peripheral nociceptive pain. We hypothesized that the inflammatory response to diffuse traumatic brain injury potentiates persistent pain through prolonged immune dysregulation. Results To test this, adult, male C57BL/6 mice were subjected to midline fluid percussion brain injury or to sham procedure. One cohort of mice was analyzed for inflammation-related cytokine levels in cortical biopsies and serum along an acute time course. In a second cohort, peripheral inflammation was induced seven days after surgery/injury with an intraplantar injection of carrageenan. This was followed by measurement of mechanical hyperalgesia, glial fibrillary acidic protein and Iba1 immunohistochemical analysis of neuroinflammation in the brain, and flow cytometric analysis of T-cell differentiation in mucosal lymph. Traumatic brain injury increased interleukin-6 and chemokine ligand 1 levels in the cortex and serum that peaked within 1–9 h and then resolved. Intraplantar carrageenan produced mechanical hyperalgesia that was potentiated by traumatic brain injury. Further, mucosal T cells from brain-injured mice showed a distinct deficiency in the ability to differentiate into inflammation-suppressing regulatory T cells (Tregs). Conclusions We conclude that traumatic brain injury increased the inflammatory pain associated with cutaneous inflammation by contributing to systemic immune dysregulation. Regulatory T cells are immune suppressors and failure of T cells to differentiate into regulatory T cells leads to unregulated cytokine production which may contribute to the potentiation of peripheral pain through the excitation of peripheral sensory neurons. In addition, regulatory T cells are

  19. Altered Cerebellar White Matter Integrity in Patients with Mild Traumatic Brain Injury in the Acute Stage

    PubMed Central

    Wang, Zhongqiu; Wu, Wenzhong; Liu, Yongkang; Wang, Tianyao; Chen, Xiao; Zhang, Jianhua; Zhou, Guoxing; Chen, Rong

    2016-01-01

    Background and Purpose Imaging studies of traumatic brain injury demonstrate that the cerebellum is often affected. We aim to examine fractional anisotropy alteration in acute-phase mild traumatic brain injury patients in cerebellum-related white matter tracts. Materials and Methods This prospective study included 47 mild traumatic brain injury patients in the acute stage and 37 controls. MR imaging and neurocognitive tests were performed in patients within 7 days of injury. White matter integrity was examined by using diffusion tensor imaging. We used three approaches, tract-based spatial statistics, graphical-model-based multivariate analysis, and region-of-interest analysis, to detect altered cerebellar white matter integrity in mild traumatic brain injury patients. Results Results from three analysis methods were in accordance with each other, and suggested fractional anisotropy in the middle cerebellar peduncle and the pontine crossing tract was changed in the acute-phase mild traumatic brain injury patients, relative to controls (adjusted p-value < 0.05). Higher fractional anisotropy in the middle cerebellar peduncle was associated with worse performance in the fluid cognition composite (r = -0.289, p-value = 0.037). Conclusion Altered cerebellar fractional anisotropy in acute-phase mild traumatic brain injury patients is localized in specific regions and statistically associated with cognitive deficits detectable on neurocognitive testing. PMID:26967320

  20. Experimental traumatic brain injury alters ethanol consumption and sensitivity.

    PubMed

    Lowing, Jennifer L; Susick, Laura L; Caruso, James P; Provenzano, Anthony M; Raghupathi, Ramesh; Conti, Alana C

    2014-10-15

    Altered alcohol consumption patterns after traumatic brain injury (TBI) can lead to significant impairments in TBI recovery. Few preclinical models have been used to examine alcohol use across distinct phases of the post-injury period, leaving mechanistic questions unanswered. To address this, the aim of this study was to describe the histological and behavioral outcomes of a noncontusive closed-head TBI in the mouse, after which sensitivity to and consumption of alcohol were quantified, in addition to dopaminergic signaling markers. We hypothesized that TBI would alter alcohol consumption patterns and related signal transduction pathways that were congruent to clinical observations. After midline impact to the skull, latency to right after injury, motor deficits, traumatic axonal injury, and reactive astrogliosis were evaluated in C57BL/6J mice. Amyloid precursor protein (APP) accumulation was observed in white matter tracts at 6, 24, and 72 h post-TBI. Increased intensity of glial fibrillary acidic protein (GFAP) immunoreactivity was observed by 24 h, primarily under the impact site and in the nucleus accumbens, a striatal subregion, as early as 72 h, persisting to 7 days, after TBI. At 14 days post-TBI, when mice were tested for ethanol sensitivity after acute high-dose ethanol (4 g/kg, intraperitoneally), brain-injured mice exhibited increased sedation time compared with uninjured mice, which was accompanied by deficits in striatal dopamine- and cAMP-regulated neuronal phosphoprotein, 32 kDa (DARPP-32) phosphorylation. At 17 days post-TBI, ethanol intake was assessed using the Drinking-in-the-Dark paradigm. Intake across 7 days of consumption was significantly reduced in TBI mice compared with sham controls, paralleling the reduction in alcohol consumption observed clinically in the initial post-injury period. These data demonstrate that TBI increases sensitivity to ethanol-induced sedation and affects downstream signaling mediators of striatal

  1. Inflicted traumatic brain injury: advances in evaluation and collaborative diagnosis.

    PubMed

    Glick, Jill C; Staley, Kelley

    2007-01-01

    The determination that a traumatic brain injury is not accidental requires data collection from multiple domains: historical, clinical, laboratory, radiographic, environmental and psychosocial. These essential, yet disparate, types of information must be synthesized in a collaborative and interdisciplinary process to formulate a medical opinion with regard to the cause of an injury, and the final opinion has tremendous consequences for children and families. Medically directed child protection teams have emerged as the standard of care in many children's hospitals and child abuse pediatrics is now a recognized medical subspecialty with board certification available in the next several years. Not only do the child and family benefit from this coordinated effort, but there are also great benefits for the members of the child protection team: more clearly defined responsibilities, redirected focus on treatment for the surgeon, and increased confidence that the opinion is based upon consensus and current scientific knowledge. By this process and its division of labor, the child abuse pediatrician assumes responsibility for ensuring that a final medical opinion is arrived at, and then advocates for appropriate disposition for the child. The child abuse pediatrician is responsible for establishing institutional standards for family evaluation, collecting all necessary medical data and directing a consensus-based decision making process that is based upon current medical knowledge, medical literature and experience. The child abuse pediatrician also assumes the role of primary communication conduit for investigational agencies and the courts. The neurosurgeon is a key member of the child protection team and relies on the team to obtain necessary historical information to address consistency of the mechanism with the sustained injuries and has an integral role in determining the team's final opinion. An interdisciplinary response to inflicted traumatic brain injury is the

  2. Predicting institutionalization after traumatic brain injury inpatient rehabilitation.

    PubMed

    Eum, Regina S; Seel, Ronald T; Goldstein, Richard; Brown, Allen W; Watanabe, Thomas K; Zasler, Nathan D; Roth, Elliot J; Zafonte, Ross D; Glenn, Mel B

    2015-02-15

    Risk factors contributing to institutionalization after inpatient rehabilitation for people with traumatic brain injury (TBI) have not been well studied and need to be better understood to guide clinicians during rehabilitation. We aimed to develop a prognostic model that could be used at admission to inpatient rehabilitation facilities to predict discharge disposition. The model could be used to provide the interdisciplinary team with information regarding aspects of patients' functioning and/or their living situation that need particular attention during inpatient rehabilitation if institutionalization is to be avoided. The study population included 7219 patients with moderate-severe TBI in the Traumatic Brain Injury Model Systems (TBIMS) National Database enrolled from 2002-2012 who had not been institutionalized prior to injury. Based on institutionalization predictors in other populations, we hypothesized that among people who had lived at a private residence prior to injury, greater dependence in locomotion, bed-chair-wheelchair transfers, bladder and bowel continence, feeding, and comprehension at admission to inpatient rehabilitation programs would predict institutionalization at discharge. Logistic regression was used, with adjustment for demographic factors, proxy measures for TBI severity, and acute-care length-of-stay. C-statistic and predictiveness curves validated a five-variable model. Higher levels of independence in bladder management (adjusted odds ratio [OR], 0.88; 95% CI 0.83, 0.93), bed-chair-wheelchair transfers (OR, 0.81 [95% CI, 0.83-0.93]), and comprehension (OR, 0.78 [95% CI, 0.68, 0.89]) at admission were associated with lower risks of institutionalization on discharge. For every 10-year increment in age was associated with a 1.38 times higher risk for institutionalization (95% CI, 1.29, 1.48) and living alone was associated with a 2.34 times higher risk (95% CI, 1.86, 2.94). The c-statistic was 0.780. We conclude that this simple model

  3. Reversing brain damage in former NFL players: implications for traumatic brain injury and substance abuse rehabilitation.

    PubMed

    Amen, Daniel G; Wu, Joseph C; Taylor, Derek; Willeumier, Kristen

    2011-01-01

    Brain injuries are common in professional American football players. Finding effective rehabilitation strategies can have widespread implications not only for retired players but also for patients with traumatic brain injury and substance abuse problems. An open label pragmatic clinical intervention was conducted in an outpatient neuropsychiatric clinic with 30 retired NFL players who demonstrated brain damage and cognitive impairment. The study included weight loss (if appropriate); fish oil (5.6 grams a day); a high-potency multiple vitamin; and a formulated brain enhancement supplement that included nutrients to enhance blood flow (ginkgo and vinpocetine), acetylcholine (acetyl-l-carnitine and huperzine A), and antioxidant activity (alpha-lipoic acid and n-acetyl-cysteine). The trial average was six months. Outcome measures were Microcog Assessment of Cognitive Functioning and brain SPECT imaging. In the retest situation, corrected for practice effect, there were statistically significant increases in scores of attention, memory, reasoning, information processing speed and accuracy on the Microcog. The brain SPECT scans, as a group, showed increased brain perfusion, especially in the prefrontal cortex, parietal lobes, occipital lobes, anterior cingulate gyrus and cerebellum. This study demonstrates that cognitive and cerebral blood flow improvements are possible in this group with multiple interventions.

  4. Primary Blast-Induced Traumatic Brain Injury in Rats Leads to Increased Prion Protein in Plasma: A Potential Biomarker for Blast-Induced Traumatic Brain Injury

    PubMed Central

    Pham, Nam; Sawyer, Thomas W.; Wang, Yushan; Jazii, Ferdous Rastgar; Vair, Cory

    2015-01-01

    Abstract Traumatic brain injury (TBI) is deemed the “signature injury” of recent military conflicts in Afghanistan and Iraq, largely because of increased blast exposure. Injuries to the brain can often be misdiagnosed, leading to further complications in the future. Therefore, the use of protein biomarkers for the screening and diagnosis of TBI is urgently needed. In the present study, we have investigated the plasma levels of soluble cellular prion protein (PrPC) as a novel biomarker for the diagnosis of primary blast-induced TBI (bTBI). We hypothesize that the primary blast wave can disrupt the brain and dislodge extracellular localized PrPC, leading to a rise in concentration within the systemic circulation. Adult male Sprague–Dawley rats were exposed to single pulse shockwave overpressures of varying intensities (15-30 psi or 103.4–206.8 kPa] using an advanced blast simulator. Blood plasma was collected 24 h after insult, and PrPC concentration was determined with a modified commercial enzyme-linked immunosorbent assay (ELISA) specific for PrPC. We provide the first report that mean PrPC concentration in primary blast exposed rats (3.97 ng/mL±0.13 SE) is significantly increased compared with controls (2.46 ng/mL±0.14 SE; two tailed test p<0.0001). Furthermore, we report a mild positive rank correlation between PrPC concentration and increasing blast intensity (psi) reflecting a plateaued response at higher pressure magnitudes, which may have implications for all military service members exposed to blast events. In conclusion, it appears that plasma levels of PrPC may be a novel biomarker for the detection of primary bTBI. PMID:25058115

  5. Traumatic Brain Injury and Neuronal Functionality Changes in Sensory Cortex

    PubMed Central

    Carron, Simone F.; Alwis, Dasuni S.; Rajan, Ramesh

    2016-01-01

    Traumatic brain injury (TBI), caused by direct blows to the head or inertial forces during relative head-brain movement, can result in long-lasting cognitive and motor deficits which can be particularly consequential when they occur in young people with a long life ahead. Much is known of the molecular and anatomical changes produced in TBI but much less is known of the consequences of these changes to neuronal functionality, especially in the cortex. Given that much of our interior and exterior lives are dependent on responsiveness to information from and about the world around us, we have hypothesized that a significant contributor to the cognitive and motor deficits seen after TBI could be changes in sensory processing. To explore this hypothesis, and to develop a model test system of the changes in neuronal functionality caused by TBI, we have examined neuronal encoding of simple and complex sensory input in the rat’s exploratory and discriminative tactile system, the large face macrovibrissae, which feeds to the so-called “barrel cortex” of somatosensory cortex. In this review we describe the short-term and long-term changes in the barrel cortex encoding of whisker motion modeling naturalistic whisker movement undertaken by rats engaged in a variety of tasks. We demonstrate that the most common form of TBI results in persistent neuronal hyperexcitation specifically in the upper cortical layers, likely due to changes in inhibition. We describe the types of cortical inhibitory neurons and their roles and how selective effects on some of these could produce the particular forms of neuronal encoding changes described in TBI, and then generalize to compare the effects on inhibition seen in other forms of brain injury. From these findings we make specific predictions as to how non-invasive extra-cranial electrophysiology can be used to provide the high-precision information needed to monitor and understand the temporal evolution of changes in neuronal

  6. Neuroendocrine abnormalities in patients with traumatic brain injury

    NASA Technical Reports Server (NTRS)

    Yuan, X. Q.; Wade, C. E.

    1991-01-01

    This article provides an overview of hypothalamic and pituitary alterations in brain trauma, including the incidence of hypothalamic-pituitary damage, injury mechanisms, features of the hypothalamic-pituitary defects, and major hypothalamic-pituitary disturbances in brain trauma. While hypothalamic-pituitary lesions have been commonly described at postmortem examination, only a limited number of clinical cases of traumatic hypothalamic-pituitary dysfunction have been reported, probably because head injury of sufficient severity to cause hypothalamic and pituitary damage usually leads to early death. With the improvement in rescue measures, an increasing number of severely head-injured patients with hypothalamic-pituitary dysfunction will survive to be seen by clinicians. Patterns of endocrine abnormalities following brain trauma vary depending on whether the injury site is in the hypothalamus, the anterior or posterior pituitary, or the upper or lower portion of the pituitary stalk. Injury predominantly to the hypothalamus can produce dissociated ACTH-cortisol levels with no response to insulin-induced hypoglycemia and a limited or failed metopirone test, hypothyroxinemia with a preserved thyroid-stimulating hormone response to thyrotropin-releasing hormone, low gonadotropin levels with a normal response to gonadotropin-releasing hormone, a variable growth hormone (GH) level with a paradoxical rise in GH after glucose loading, hyperprolactinemia, the syndrome of inappropriate ADH secretion (SIADH), temporary or permanent diabetes insipidus (DI), disturbed glucose metabolism, and loss of body temperature control. Severe damage to the lower pituitary stalk or anterior lobe can cause low basal levels of all anterior pituitary hormones and eliminate responses to their releasing factors. Only a few cases showed typical features of hypothalamic or pituitary dysfunction. Most severe injuries are sufficient to damage both structures and produce a mixed endocrine picture

  7. Functional Integration of Adult-Born Hippocampal Neurons after Traumatic Brain Injury

    PubMed Central

    Villasana, Laura E.; Kim, Kristine N.

    2015-01-01

    Abstract Traumatic brain injury (TBI) increases hippocampal neurogenesis, which may contribute to cognitive recovery after injury. However, it is unknown whether TBI-induced adult-born neurons mature normally and functionally integrate into the hippocampal network. We assessed the generation, morphology, and synaptic integration of new hippocampal neurons after a controlled cortical impact (CCI) injury model of TBI. To label TBI-induced newborn neurons, we used 2-month-old POMC-EGFP mice, which transiently and specifically express EGFP in immature hippocampal neurons, and doublecortin-CreERT2 transgenic mice crossed with Rosa26-CAG-tdTomato reporter mice, to permanently pulse-label a cohort of adult-born hippocampal neurons. TBI increased the generation, outward migration, and dendritic complexity of neurons born during post-traumatic neurogenesis. Cells born after TBI had profound alterations in their dendritic structure, with increased dendritic branching proximal to the soma and widely splayed dendritic branches. These changes were apparent during early dendritic outgrowth and persisted as these cells matured. Whole-cell recordings from neurons generated during post-traumatic neurogenesis demonstrate that they are excitable and functionally integrate into the hippocampal circuit. However, despite their dramatic morphologic abnormalities, we found no differences in the rate of their electrophysiological maturation, or their overall degree of synaptic integration when compared to age-matched adult-born cells from sham mice. Our results suggest that cells born after TBI participate in information processing, and receive an apparently normal balance of excitatory and inhibitory inputs. However, TBI-induced changes in their anatomic localization and dendritic projection patterns could result in maladaptive network properties. PMID:26478908

  8. Contribution of psychological trauma to outcomes after traumatic brain injury: assaults versus sporting injuries.

    PubMed

    Mathias, Jane L; Harman-Smith, Yasmin; Bowden, Stephen C; Rosenfeld, Jeffrey V; Bigler, Erin D

    2014-04-01

    Clinical research into outcomes after traumatic brain injury (TBI) frequently combines injuries that have been sustained through different causes (e.g., car accidents, assaults, and falls), the effect of which is not well understood. This study examined the contribution of injury-related psychological trauma—which is more commonly associated with specific types of injuries—to outcomes after nonpenetrating TBI in order to determine whether it may be having a differential effect in samples containing mixed injuries. Data from three groups that were prospectively recruited for two larger studies were compared: one that sustained a TBI as a result of physical assaults (i.e., psychologically traumatizing) and another as a result of sporting injuries (i.e., nonpsychologically traumatizing), as well as an orthopedic control group (OC). Psychosocial and emotional (postconcussion symptoms, injury-related stress, and depression), cognitive (memory, abstract reasoning, problem solving, and verbal fluency), and functional (general outcome; resumption of home, social, and work roles) outcomes were all assessed. The TBI(assault) group reported significantly poorer psychosocial and emotional outcomes and higher rates of litigation (criminal rather than civil) than both the TBI(sport) and OC groups approximately 6 months postinjury, but there were no differences in the cognitive or functional outcomes of the three groups. The findings suggest that the cause of a TBI may assist in explaining some of the differences in outcomes of people who have seemingly comparable injuries. Involvement in litigation and the cause of an injury may also be confounded, which may lead to the erroneous conclusion that litigants have poorer outcomes.

  9. Early Exposure to Traumatic Stressors Impairs Emotional Brain Circuitry

    PubMed Central

    Korgaonkar, Mayuresh S.; Antees, Cassandra; Williams, Leanne M.; Gatt, Justine M.; Bryant, Richard A.; Cohen, Ronald; Paul, Robert; O’Hara, Ruth; Grieve, Stuart M.

    2013-01-01

    Exposure to early life trauma (ELT) is known to have a profound impact on mental development, leading to a higher risk for depression and anxiety. Our aim was to use multiple structural imaging methods to systematically investigate how traumatic stressors early in life impact the emotional brain circuits, typically found impaired with clinical diagnosis of depression and anxiety, across the lifespan in an otherwise healthy cohort. MRI data and self-reported histories of ELT from 352 healthy individuals screened for no psychiatric disorders were analyzed in this study. The volume and cortical thickness of the limbic and cingulate regions were assessed for all participants. A large subset of the cohort also had diffusion tensor imaging data, which was used to quantify white matter structural integrity of these regions. We found a significantly smaller amygdala volume and cortical thickness in the rostral anterior cingulate cortex associated with higher ELT exposure only for the adolescence group. White matter integrity of these regions was not affected. These findings demonstrate that exposure to early life trauma is associated with alterations in the gray matter of cingulate-limbic regions during adolescence in an otherwise healthy sample. These findings are interesting in the context that the affected regions are central neuroanatomical components in the psychopathology of depression, and adolescence is a peak period for risk and onset of the disorder. PMID:24073270

  10. Attention remediation following traumatic brain injury in childhood and adolescence.

    PubMed

    Galbiati, Susanna; Recla, Monica; Pastore, Valentina; Liscio, Mariarosaria; Bardoni, Alessandra; Castelli, Enrico; Strazzer, Sandra

    2009-01-01

    Traumatic brain injury (TBI) frequently affects both the basic and the superordinate components of attention; deficits vary according to patient age. This study evaluated the efficacy of a specific remediation intervention for attention. Sixty-five TBI patients (aged 6?18 years) with attention deficit were assessed at baseline and at 1-year follow-up: 40 patients received attention-specific neuropsychological training for 6 months, and the control group comprised 25 patients. Cognitive assessment included a Wechsler Intelligence Scale (e.g., A. Orsini, 1993) and the Continuous Performance Test II (CPT II; C. K. Conners, 2000). The Vineland Adaptive Behavior Scales (VABS; S. Sparrow, D. Balla & D. V. Cicchetti, 1984) was administered to assess the treatment's ecological validity. At baseline, all patients presented with a mild intellectual disability and pathological scores on the CPT II. At follow-up, significant differences were found between the 2 groups on the CPT II and VABS: The clinical group improved more than the control group. Specific remediation training for attention, including a combination of a process-specific approach and metacognitive strategies, significantly improved attention performance. Improvement in attention skills also affected adaptive skills positively.

  11. Sleep and wake disturbances following traumatic brain injury.

    PubMed

    Duclos, C; Dumont, M; Wiseman-Hakes, C; Arbour, C; Mongrain, V; Gaudreault, P-O; Khoury, S; Lavigne, G; Desautels, A; Gosselin, N

    2014-10-01

    Traumatic brain injury (TBI) is a major health concern in industrialised countries. Sleep and wake disturbances are among the most persistent and disabling sequelae after TBI. Yet, despite the widespread complaints of post-TBI sleep and wake disturbances, studies on their etiology, pathophysiology, and treatments remain inconclusive. This narrative review aims to summarise the current state of knowledge regarding the nature of sleep and wake disturbances following TBI, both subjective and objective, spanning all levels of severity and phases post-injury. A second goal is to outline the various causes of post-TBI sleep-wake disturbances. Globally, although sleep-wake complaints are reported in all studies and across all levels of severity, consensus regarding the objective nature of these disturbances is not unanimous and varies widely across studies. In order to optimise recovery in TBI survivors, further studies are required to shed light on the complexity and heterogeneity of post-TBI sleep and wake disturbances, and to fully grasp the best timing and approach for intervention.

  12. Effect of marijuana use on outcomes in traumatic brain injury.

    PubMed

    Nguyen, Brian M; Kim, Dennis; Bricker, Scott; Bongard, Fred; Neville, Angela; Putnam, Brant; Smith, Jennifer; Plurad, David

    2014-10-01

    Traumatic brain injury (TBI) is associated with significant morbidity and mortality. Several studies have demonstrated neuroprotective effects of cannabinoids. The objective of this study was to establish a relationship between the presence of a positive toxicology screen for tetrahydrocannabinol (THC) and mortality after TBI. A 3-year retrospective review of registry data at a Level I center of patients sustaining TBI having a toxicology screen was performed. Pediatric patients (younger than 15 years) and patients with a suspected nonsurvivable injury were excluded. The THC(+) group was compared with the THC(-) group with respect to injury mechanism, severity, disposition, and mortality. Logistic regression was used to determine independent associations with mortality. There were 446 cases meeting all inclusion criteria. The incidence of a positive THC screen was 18.4 per cent (82). Overall mortality was 9.9 per cent (44); however, mortality in the THC(+) group (2.4% [two]) was significantly decreased compared with the THC(-) group (11.5% [42]; P = 0.012). After adjusting for differences between the study cohorts on logistic regression, a THC(+) screen was independently associated with survival after TBI (odds ratio, 0.224; 95% confidence interval, 0.051 to 0.991; P = 0.049). A positive THC screen is associated with decreased mortality in adult patients sustaining TBI. PMID:25264643

  13. Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury

    PubMed Central

    Reifschneider, Kent; Auble, Bethany A.; Rose, Susan R.

    2015-01-01

    Traumatic brain injuries (TBI) are common occurrences in childhood, often resulting in long term, life altering consequences. Research into endocrine sequelae following injury has gained attention; however, there are few studies in children. This paper reviews the pathophysiology and current literature documenting risk for endocrine dysfunction in children suffering from TBI. Primary injury following TBI often results in disruption of the hypothalamic-pituitary-adrenal axis and antidiuretic hormone production and release, with implications for both acute management and survival. Secondary injuries, occurring hours to weeks after TBI, result in both temporary and permanent alterations in pituitary function. At five years after moderate to severe TBI, nearly 30% of children suffer from hypopituitarism. Growth hormone deficiency and disturbances in puberty are the most common; however, any part of the hypothalamic-pituitary axis can be affected. In addition, endocrine abnormalities can improve or worsen with time, having a significant impact on children’s quality of life both acutely and chronically. Since primary and secondary injuries from TBI commonly result in transient or permanent hypopituitarism, we conclude that survivors should undergo serial screening for possible endocrine disturbances. High indices of suspicion for life threatening endocrine deficiencies should be maintained during acute care. Additionally, survivors of TBI should undergo endocrine surveillance by 6–12 months after injury, and then yearly, to ensure early detection of deficiencies in hormonal production that can substantially influence growth, puberty and quality of life. PMID:26287247

  14. Monitoring of Intracranial Pressure in Patients with Traumatic Brain Injury

    PubMed Central

    Hawthorne, Christopher; Piper, Ian

    2014-01-01

    Since Monro published his observations on the nature of the contents of the intracranial space in 1783, there has been investigation of the unique relationship between the contents of the skull and the intracranial pressure (ICP). This is particularly true following traumatic brain injury (TBI), where it is clear that elevated ICP due to the underlying pathological processes is associated with a poorer clinical outcome. Consequently, there is considerable interest in monitoring and manipulating ICP in patients with TBI. The two techniques most commonly used in clinical practice to monitor ICP are via an intraventricular or intraparenchymal catheter with a microtransducer system. Both of these techniques are invasive and are thus associated with complications such as hemorrhage and infection. For this reason, significant research effort has been directed toward development of a non-invasive method to measure ICP. The principle aims of ICP monitoring in TBI are to allow early detection of secondary hemorrhage and to guide therapies that limit intracranial hypertension (ICH) and optimize cerebral perfusion. However, information from the ICP value and the ICP waveform can also be used to assess the intracranial volume–pressure relationship, estimate cerebrovascular pressure reactivity, and attempt to forecast future episodes of ICH. PMID:25076934

  15. Self-awareness and traumatic brain injury outcome

    PubMed Central

    Robertson, Kayela; Schmitter-Edgecombe, Maureen

    2016-01-01

    Primary Objective Impaired self-awareness following a traumatic brain injury (TBI) can reduce the effectiveness of rehabilitation, resulting in poorer outcomes. However, little is understood about how the multi-dimensional aspects of self-awareness may differentially change with recovery and impact outcome. Thus, we examined four self-awareness variables represented in the Dynamic Comprehensive Model of Awareness: metacognitive awareness, anticipatory awareness, error-monitoring, and self-regulation. Research Design We evaluated change of the self-awareness measures with recovery from TBI and whether the self-awareness measures predicted community reintegration at follow-up. Methods and Procedures Participants were 90 individuals with moderate to severe TBI who were tested acutely following injury and 90 age-matched controls. Forty-nine of the TBI participants and 49 controls were re-tested after 6 months. Main Outcome and Results Results revealed that the TBI group’s error-monitoring performance was significantly poorer than controls at both baseline and follow-up. Regression analyses revealed that the self-awareness variables at follow-up were predictive of community reintegration, with error-monitoring being a unique predictor. Conclusions Our results highlight the importance of error-monitoring and suggest that interventions targeted at improving error-monitoring may be particularly beneficial. Understanding the multi-dimensional nature of self-awareness will further improve rehabilitation efforts and understanding of the theoretical basis of self-awareness. PMID:25915097

  16. Traumatic brain injury: endocrine consequences in children and adults.

    PubMed

    Richmond, Erick; Rogol, Alan D

    2014-02-01

    Traumatic brain injury (TBI) is a common cause of death and disability in young adults with consequences ranging from physical disabilities to long-term cognitive, behavioral, psychological and social defects. Recent data suggest that pituitary hormone deficiency is not infrequent among TBI survivors; the prevalence of reported hypopituitarism following TBI varies widely among published studies. The most common cause of TBI is motor vehicle accidents, including pedestrian-car and bicycle car encounters, falls, child abuse, violence and sports injuries. Prevalence of hypopituitarism, from total to isolated pituitary deficiency, ranges from 5 to 90 %. The time interval between TBI and pituitary function evaluation is one of the major factors responsible for variations in the prevalence of hypopituitarism reported. Endocrine dysfunction after TBI in children and adolescents is common. Adolescence is a time of growth, freedom and adjustment, consequently TBI is also common in this group. Sports-related TBI is an important public health concern, but many cases are unrecognized and unreported. Sports that are associated with an increased risk of TBI include those involving contact and/or collisions such as boxing, football, soccer, ice hockey, rugby, and the martial arts, as well as high velocity sports such as cycling, motor racing, equestrian sports, skiing and roller skating. The aim of this paper is to summarize the best evidence of TBI as a cause of pituitary deficiency in children and adults. PMID:24030696

  17. Communication after mild traumatic brain injury--a spouse's perspective.

    PubMed

    Crewe-Brown, Samantha Jayne; Stipinovich, Alexandra Maria; Zsilavecz, Ursula

    2011-10-01

    Individuals with mild traumatic brain injury (MTBI) often perform within normal limits on linguistic and cognitive assessments. However, they may present with debilitating communicative difficulties in daily life. A multifaceted approach to MTBI with a focus on everyday communication in natural settings is required. Significant others who interact with the individual with MTBI in a variety of settings may be sensitive to communicative difficulties experienced by the individual with MTBI. This article examines communication after MTBI from the perspective of the spouse. A case study design was implemented. The spouses of two individuals with MTBI served as the participants for this study. Semi-structured interviews were held, during which each participant was requested to describe the communication of their spouse with MTBI. The content obtained from the interviews was subjected to a discourse analysis. The results show that both participants perceived changes in the communication of their spouse following the MTBI. The results further show that MTBI affected communication of the two individuals in different ways. The value of a 'significant other' in providing information regarding communication in natural settings is highlighted. The implications of these findings for the assessment and management of the communication difficulties associated with MTBI are discussed. PMID:22216558

  18. Cytokine gene polymorphisms and outcome after traumatic brain injury.

    PubMed

    Waters, Ryan J; Murray, Gordon D; Teasdale, Graham M; Stewart, Janice; Day, Ian; Lee, Robert J; Nicoll, James A R

    2013-10-15

    Clinical outcome after traumatic brain injury (TBI) is variable and cannot easily be predicted. There is increasing evidence to suggest that there may be genetic influences on outcome. Cytokines play an important role in mediating the inflammatory response provoked within the central nervous system after TBI. This study was designed to identify associations between cytokine gene polymorphisms and clinical outcome 6 months after head injury. A prospectively identified cohort of patients (n=1096, age range 0-93 years, mean age 37) was used. Clinical outcome at 6 months was assessed using the Glasgow Outcome Scale. In an initial screen of 11 cytokine gene single nucleotide polymorphisms (SNPs) previously associated with disease susceptibility or outcome (TNFA -238 and -308, IL6 -174, -572 and -597, IL1A -889, IL1B -31, -511 and +3953, and TGFB -509 and -800), TNFA -308 was identified as having a likely association. The TNFA -308 SNP was further evaluated, and a significant association was identified, with 39% of allele 2 carriers having an unfavorable outcome compared with 31% of non-carriers (adjusted odds ratio 1.67, confidence interval 1.19-2.35, p=0.003). These findings are consistent with experimental and clinical data suggesting that neuroinflammation has an impact on clinical outcome after TBI and that tumor necrosis factor alpha plays an important role in this process.

  19. Pain Catastrophizing Correlates with Early Mild Traumatic Brain Injury Outcome

    PubMed Central

    Chaput, Geneviève; Lajoie, Susanne P.; Naismith, Laura M.; Lavigne, Gilles

    2016-01-01

    Background. Identifying which patients are most likely to be at risk of chronic pain and other postconcussion symptoms following mild traumatic brain injury (MTBI) is a difficult clinical challenge. Objectives. To examine the relationship between pain catastrophizing, defined as the exaggerated negative appraisal of a pain experience, and early MTBI outcome. Methods. This cross-sectional design included 58 patients diagnosed with a MTBI. In addition to medical chart review, postconcussion symptoms were assessed by self-report at 1 month (Time 1) and 8 weeks (Time 2) after MTBI. Pain severity, psychological distress, level of functionality, and pain catastrophizing were measured by self-report at Time 2. Results. The pain catastrophizing subscales of rumination, magnification, and helplessness were significantly correlated with pain severity (r = .31 to .44), number of postconcussion symptoms reported (r = .35 to .45), psychological distress (r = .57 to .67), and level of functionality (r = −.43 to −.29). Pain catastrophizing scores were significantly higher for patients deemed to be at high risk of postconcussion syndrome (6 or more symptoms reported at both Time 1 and Time 2). Conclusions. Higher levels of pain catastrophizing were related to adverse early MTBI outcomes. The early detection of pain catastrophizing may facilitate goal-oriented interventions to prevent or minimize the development of chronic pain and other postconcussion symptoms. PMID:27445604

  20. Cardiac reactive oxygen species after traumatic brain injury

    PubMed Central

    Larson, Brett E; Stockwell, David W.; Boas, Stefan; Andrews, Trevor; Wellman, George C.; Lockette, Warren; Freeman, Kalev

    2011-01-01

    Background Cardiovascular complications after traumatic brain injury (TBI) contribute to morbidity and mortality and may provide a target for therapy. We examined blood pressure and left ventricle contractility after TBI, and tested the hypothesis that beta-adrenergic blockade would decrease oxidative stress after TBI. Material and Methods Rodents received fluid-percussion injury or sham surgery, confirmed with magnetic resonance imaging (MRI) and histopathology. We followed recovery with sensorimotor coordination testing and blood pressure measurements. We assessed left ventricular ejection fraction using ECG-gated cardiac MRI and measured myocardial reactive oxygen species (ROS) with dihydroethidium. We randomized additional TBI and sham animals to post-operative treatment with propranolol or control, for measurement of ROS. Results Blood pressure and cardiac contractility were elevated 48 hours after TBI. Myocardial tissue sections showed increased ROS. Treatment with propranolol diminished ROS levels following TBI. Conclusions TBI is associated with increased cardiac contractility and myocardial ROS; decreased myocardial ROS after beta-blockade suggests that sympathetic stimulation is a mechanism of oxidative stress. PMID:22172132

  1. Cognitive Impairment and Rehabilitation Strategies After Traumatic Brain Injury

    PubMed Central

    Barman, Apurba; Chatterjee, Ahana; Bhide, Rohit

    2016-01-01

    Traumatic brain injury (TBI) is among the significant causes of morbidity and mortality in the present world. Around 1.6 million persons sustain TBI, whereas 200,000 die annually in India, thus highlighting the rising need for appropriate cognitive rehabilitation strategies. This literature review assesses the current knowledge of various cognitive rehabilitation training strategies. The entire spectrum of TBI severity; mild to severe, is associated with cognitive deficits of varying degree. Cognitive insufficiency is more prevalent and longer lasting in TBI persons than in the general population. A multidisciplinary approach with neuropsychiatric evaluation is warranted. Attention process training and tasks for attention deficits, compensatory strategies and errorless learning training for memory deficits, pragmatic language skills and social behavior guidance for cognitive-communication disorder, meta-cognitive strategy, and problem-solving training for executive disorder are the mainstay of therapy for cognitive deficits in persons with TBI. Cognitive impairments following TBI are common and vary widely. Different cognitive rehabilitation techniques and combinations in addition to pharmacotherapy are helpful in addressing various cognitive deficits. PMID:27335510

  2. Cognitive Impairment and Rehabilitation Strategies After Traumatic Brain Injury.

    PubMed

    Barman, Apurba; Chatterjee, Ahana; Bhide, Rohit

    2016-01-01

    Traumatic brain injury (TBI) is among the significant causes of morbidity and mortality in the present world. Around 1.6 million persons sustain TBI, whereas 200,000 die annually in India, thus highlighting the rising need for appropriate cognitive rehabilitation strategies. This literature review assesses the current knowledge of various cognitive rehabilitation training strategies. The entire spectrum of TBI severity; mild to severe, is associated with cognitive deficits of varying degree. Cognitive insufficiency is more prevalent and longer lasting in TBI persons than in the general population. A multidisciplinary approach with neuropsychiatric evaluation is warranted. Attention process training and tasks for attention deficits, compensatory strategies and errorless learning training for memory deficits, pragmatic language skills and social behavior guidance for cognitive-communication disorder, meta-cognitive strategy, and problem-solving training for executive disorder are the mainstay of therapy for cognitive deficits in persons with TBI. Cognitive impairments following TBI are common and vary widely. Different cognitive rehabilitation techniques and combinations in addition to pharmacotherapy are helpful in addressing various cognitive deficits. PMID:27335510

  3. Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury.

    PubMed

    Reifschneider, Kent; Auble, Bethany A; Rose, Susan R

    2015-01-01

    Traumatic brain injuries (TBI) are common occurrences in childhood, often resulting in long term, life altering consequences. Research into endocrine sequelae following injury has gained attention; however, there are few studies in children. This paper reviews the pathophysiology and current literature documenting risk for endocrine dysfunction in children suffering from TBI. Primary injury following TBI often results in disruption of the hypothalamic-pituitary-adrenal axis and antidiuretic hormone production and release, with implications for both acute management and survival. Secondary injuries, occurring hours to weeks after TBI, result in both temporary and permanent alterations in pituitary function. At five years after moderate to severe TBI, nearly 30% of children suffer from hypopituitarism. Growth hormone deficiency and disturbances in puberty are the most common; however, any part of the hypothalamic-pituitary axis can be affected. In addition, endocrine abnormalities can improve or worsen with time, having a significant impact on children's quality of life both acutely and chronically. Since primary and secondary injuries from TBI commonly result in transient or permanent hypopituitarism, we conclude that survivors should undergo serial screening for possible endocrine disturbances. High indices of suspicion for life threatening endocrine deficiencies should be maintained during acute care. Additionally, survivors of TBI should undergo endocrine surveillance by 6-12 months after injury, and then yearly, to ensure early detection of deficiencies in hormonal production that can substantially influence growth, puberty and quality of life. PMID:26287247

  4. Pathophysiology and Treatment of Severe Traumatic Brain Injuries in Children.

    PubMed

    Allen, Kimberly A

    2016-02-01

    Traumatic brain injuries (TBIs) in children are a major cause of morbidity and mortality worldwide. Severe TBIs account for 15,000 admissions annually and a mortality rate of 24% in children in the United States. The purpose of this article is to explore pathophysiologic events, examine monitoring techniques, and explain current treatment modalities and nursing care related to caring for children with severe TBI. The primary injury of a TBI is because of direct trauma from an external force, a penetrating object, blast waves, or a jolt to the head. Secondary injury occurs because of alterations in cerebral blood flow, and the development of cerebral edema leads to necrotic and apoptotic cellular death after TBI. Monitoring focuses on intracranial pressure, cerebral oxygenation, cerebral edema, and cerebrovascular injuries. If abnormalities are identified, treatments are available to manage the negative effects caused to the cerebral tissue. The mainstay treatments are hyperosmolar therapy; temperature control; cerebrospinal fluid drainage; barbiturate therapy; decompressive craniectomy; analgesia, sedation, and neuromuscular blockade; and antiseizure prophylaxis. PMID:26720317

  5. Transcranial magnetic stimulation facilitates neurorehabilitation after pediatric traumatic brain injury

    PubMed Central

    Lu, Hongyang; Kobilo, Tali; Robertson, Courtney; Tong, Shanbao; Celnik, Pablo; Pelled, Galit

    2015-01-01

    Traumatic brain injury (TBI) is the leading cause of death and disability among children in the United States. Affected children will often suffer from emotional, cognitive and neurological impairments throughout life. In the controlled cortical impact (CCI) animal model of pediatric TBI (postnatal day 16–17) it was demonstrated that injury results in abnormal neuronal hypoactivity in the non-injured primary somatosensory cortex (S1). It materializes that reshaping the abnormal post-injury neuronal activity may provide a suitable strategy to augment rehabilitation. We tested whether high-frequency, non-invasive transcranial magnetic stimulation (TMS) delivered twice a week over a four-week period can rescue the neuronal activity and improve the long-term functional neurophysiological and behavioral outcome in the pediatric CCI model. The results show that TBI rats subjected to TMS therapy showed significant increases in the evoked-fMRI cortical responses (189%), evoked synaptic activity (46%), evoked neuronal firing (200%) and increases expression of cellular markers of neuroplasticity in the non-injured S1 compared to TBI rats that did not receive therapy. Notably, these rats showed less hyperactivity in behavioral tests. These results implicate TMS as a promising approach for reversing the adverse neuronal mechanisms activated post-TBI. Importantly, this intervention could readily be translated to human studies. PMID:26440604

  6. Irony and empathy in children with traumatic brain injury.

    PubMed

    Dennis, Maureen; Simic, Nevena; Agostino, Alba; Taylor, H Gerry; Bigler, Erin D; Rubin, Kenneth; Vannatta, Kathryn; Gerhardt, Cynthia A; Stancin, Terry; Yeates, Keith Owen

    2013-03-01

    Social communication involves influencing what other people think and feel about themselves. We use the term conative theory of mind (ToM) to refer to communicative interactions involving one person trying to influence the mental and emotional state of another, paradigmatic examples of which are irony and empathy. This study reports how children with traumatic brain injury (TBI) understand ironic criticism and empathic praise, on a task requiring them to identify speaker belief and intention for direct conative speech acts involving literal truth, and indirect speech acts involving either ironic criticism or empathic praise. Participants were 71 children in the chronic state of a single TBI and 57 age- and gender-matched children with orthopedic injuries (OI). Group differences emerged on indirect speech acts involving conation (i.e., irony and empathy), but not on structurally and linguistically identical direct speech acts, suggesting specific deficits in this aspect of social cognition in school-age children with TBI. Deficits in children with mild-moderate TBI were less widespread and more selective than those of children with more severe injuries. Deficits in understanding the social, conative function of indirect speech acts like irony and empathy have widespread and deep implications for social function in children with TBI.

  7. Cognitive correlates of narrative impairment in moderate traumatic brain injury.

    PubMed

    Marini, Andrea; Zettin, Marina; Galetto, Valentina

    2014-11-01

    Traumatic brain injuries (TBIs) are often associated with communicative deficits. The incoherent and impoverished language observed in non-aphasic individuals with severe TBI has been linked to a problem in the global organization of information at the text level. The present study aimed to analyze the features of narrative discourse impairment in a group of adults with moderate TBI (modTBI). 10 non-aphasic speakers with modTBI and 20 neurologically intact participants were recruited for the experiment. Their cognitive, linguistic and narrative skills were thoroughly assessed. The persons with modTBI exhibited normal phonological, lexical and grammatical skills. However, their narratives were characterized by lower levels of Lexical Informativeness and more errors of both Local and Global Coherence that, at times, made their narratives vague and ambiguous. Significant correlations were found between these narrative difficulties and the production of both perseverative and non-perseverative errors on the WCST. These disturbances confirm previous findings which suggest a deficit at the interface between cognitive and linguistic processing rather than a specific linguistic disturbance in these patients. PMID:25281884

  8. Diffusion tensor imaging in mild traumatic brain injury litigation.

    PubMed

    Wortzel, Hal S; Kraus, Marilyn F; Filley, Christopher M; Anderson, C Alan; Arciniegas, David B

    2011-01-01

    A growing body of literature addresses the application of diffusion tensor imaging (DTI) to traumatic brain injury (TBI). Most TBIs are of mild severity, and their diagnosis and prognosis are often challenging. These challenges may be exacerbated in medicolegal contexts, where plaintiffs seek to present objective evidence that supports a clinical diagnosis of mild (m)TBI. Because DTI permits quantification of white matter integrity and because TBI frequently involves white matter injury, DTI represents a conceptually appealing method of demonstrating white matter pathology attributable to mTBI. However, alterations in white matter integrity are not specific to TBI, and their presence does not necessarily confirm a diagnosis of mTBI. Guided by rules of evidence shaped by Daubert v. Merrell Dow Pharmaceuticals, Inc., we reviewed and analyzed the literature describing DTI findings in mTBI and related neuropsychiatric disorders. Based on this review, we suggest that expert testimony regarding DTI findings will seldom be appropriate in legal proceedings focused on mTBI. PMID:22159979

  9. Tracheal decannulation protocol in patients affected by traumatic brain injury.

    PubMed

    Zanata, Isabel de Lima; Santos, Rosane Sampaio; Hirata, Gisela Carmona

    2014-04-01

    Introduction The frequency of tracheostomy in patients with traumatic brain injury (TBI) contrasts with the lack of objective criteria for its management. The study arose from the need for a protocol in the decision to remove the tracheal tube. Objective To evaluate the applicability of a protocol for tracheal decannulation. Methods A prospective study with 20 patients, ranging between 21 and 85 years of age (average 33.55), 4 of whom were women (20%) and 16 were men (80%). All patients had been diagnosed by a neurologist as having TBI, and the anatomical region of the lesion was known. Patients were evaluated following criteria for tracheal decannulation through a clinical evaluation protocol developed by the authors. Results Decannulation was performed in 12 (60%) patients. Fourteen (70%) had a score greater than 8 on the Glasgow Coma Scale and only 2 (14%) of these were not able to undergo decannulation. Twelve (60%) patients maintained the breathing pattern with occlusion of the tube and were successfully decannulated. Of the 20 patients evaluated, 11 (55%) showed no signs suggestive of tracheal aspiration, and of these, 9 (82%) began training on occlusion of the cannula. The protocol was relevant to establish the beginning of the decannulation process. The clinical assessment should focus on the patient's condition to achieve early tracheal decannulation. Conclusion This study allowed, with the protocol, to establish six criteria for tracheal decannulation: level of consciousness, respiration, tracheal secretion, phonation, swallowing, and coughing. PMID:25992074

  10. Exploring Vocational Evaluation Practices following Traumatic Brain Injury

    PubMed Central

    Dillahunt-Aspillaga, Christina; Jorgensen Smith, Tammy; Hanson, Ardis; Ehlke, Sarah; Stergiou-Kita, Mary; Dixon, Charlotte G.; Quichocho, Davina

    2015-01-01

    Background. Individuals with traumatic brain injury (TBI) face many challenges when attempting to return to work (RTW). Vocational evaluation (VE) is a systematic process that involves assessment and appraisal of an individual's current work-related characteristics and abilities. Objective. The aims of this study are to (1) examine demographic and employment characteristics of vocational rehabilitation providers (VRPs), (2) identify the specific evaluation methods that are used in the VE of individuals with TBI, and (3) examine the differences in assessment method practices based upon evaluator assessment preferences. Methods. This exploratory case study used a forty-six-item online survey which was distributed to VRPs. Results. One hundred and nine VRPs accessed the survey. Of these, 74 completed the survey. A majority of respondents were female (79.7%), Caucasian (71.6%), and holding a master's degree (74.3%), and more than half (56.8%) were employed as state vocational rehabilitation counselors (VRCs). In addition, over two-thirds (67.6%) were certified rehabilitation counselors (CRCs). Respondents reported using several specific tools and assessments during the VE process. Conclusions. Study findings reveal differences in use of and rationales for specific assessments amongst VRPs. Understanding VRP assessment practices and use of an evidence-based framework for VE following TBI may inform and improve VE practice. PMID:26494945

  11. Ventilator-Associated Pneumonia in Pediatric Traumatic Brain Injury.

    PubMed

    Hamele, Mitchell; Stockmann, Chris; Cirulis, Meghan; Riva-Cambrin, Jay; Metzger, Ryan; Bennett, Tellen D; Bratton, Susan L

    2016-05-01

    Ventilator-associated pneumonia (VAP) is a common occurrence among intubated pediatric traumatic brain injury (TBI) patients. However, little is known about the epidemiology, risk factors, and microbiology of VAP in pediatric TBI. We reviewed a cohort of 119 pediatric moderate-to-severe TBI patients and identified 42 with VAP by positive protected bronchial brush specimens. Location of intubation, severity of injury, and antibiotic administration within 2 days after injury were not associated with VAP. Most treatments for elevated intracranial pressure were associated with increased risk of VAP; however, in a multi-variable analysis barbiturate coma (hazard ratio [HR], 3.2; 95% confidence interval [CI] 1.4-7.3), neuromuscular blockade (NMBA; HR, 3.4; 95% CI 1.6-7.3), and use of a cooling blanket for euthermia (HR 2.4; 95% CI 1.1-5.5) remained independently associated with VAP. Most VAP (55%) occurred prior to hospital Day 4 and only 7% developed VAP after Day 7. Methicillin-sensitive Staphylococcus aureus (34%), Haemophilus influenzae (22%), and Streptococcus pneumoniae (15%) were the most common organisms, comprising 71% of isolated pathogens (36% of infections were polymicrobial). Patients with VAP had significantly longer intensive care unit and hospital stays, as well as increased risk of chronic care needs after discharge, but not mortality. VAP is a common occurrence in pediatric TBI patients, and early empiric therapy for patients requiring barbiturate infusion, NMBA, or use of a cooling blanket could mitigate morbidity.

  12. External causes of traumatic brain injury, 2000-2011.

    PubMed

    2013-03-01

    This report summarizes frequencies, distributions, and trends of external causes of traumatic brain injuries (TBIs) that are recorded on standardized records of medical encounters of U.S. military members. Causes of TBI were reported for 100 percent of cases hospitalized in military facilities, but were relatively infrequently reported in other treatment settings (i.e., military outpatient facilities, combat theater and civilian medical facilities). During 2008-2011 in all clinical settings combined, 24,115 service members had TBI case-defining medical encounters with recorded injury causes. Accidents represented 74 percent of recorded causes; the most frequently reported specific causes were motor vehicle traffic accidents (20%), falls (20%), and being struck by or struck against an object (15%). Similar proportions of TBIs were reportedly due to intentional "assaults" unrelated to war (11%) and "battle injuries" (11%). Assaults were second only to motor vehicle accidents as reported causes of TBIs treated in civilian hospitals. Some TBIs reportedly due to accidents with guns/explosives were likely combat injuries that were miscoded in military hospitals. The doubling of the number of combat-related TBIs reported from Iraq/Afghanistan between 2010 and 2011 undoubtedly reflects the U.S. military's increased focus on identifying and treating TBIs among deployed military members. PMID:23550928

  13. Hypopituitarism in Traumatic Brain Injury—A Critical Note

    PubMed Central

    Klose, Marianne; Feldt-Rasmussen, Ulla

    2015-01-01

    While hypopituitarism after traumatic brain injury (TBI) was previously considered rare, it is now thought to be a major cause of treatable morbidity among TBI survivors. Consequently, recommendations for assessment of pituitary function and replacement in TBI were recently introduced. Given the high incidence of TBI with more than 100 pr. 100,000 inhabitants, TBI would be by far the most common cause of hypopituitarism if the recently reported prevalence rates hold true. The disproportion between this proposed incidence and the occasional cases of post-TBI hypopituitarism in clinical practice justifies reflection as to whether hypopituitarism has been unrecognized in TBI patients or whether diagnostic testing designed for high risk populations such as patients with obvious pituitary pathology has overestimated the true risk and thereby the disease burden of hypopituitarism in TBI. The findings on mainly isolated deficiencies in TBI patients, and particularly isolated growth hormone (GH) deficiency, raise the question of the potential impact of methodological confounding, determined by variable test-retest reproducibility, appropriateness of cut-off values, importance of BMI stratified cut-offs, assay heterogeneity, pre-test probability of hypopituitarism and lack of proper individual laboratory controls as reference population. In this review, current recommendations are discussed in light of recent available evidence. PMID:26239687

  14. Sleep and wake disturbances following traumatic brain injury.

    PubMed

    Duclos, C; Dumont, M; Wiseman-Hakes, C; Arbour, C; Mongrain, V; Gaudreault, P-O; Khoury, S; Lavigne, G; Desautels, A; Gosselin, N

    2014-10-01

    Traumatic brain injury (TBI) is a major health concern in industrialised countries. Sleep and wake disturbances are among the most persistent and disabling sequelae after TBI. Yet, despite the widespread complaints of post-TBI sleep and wake disturbances, studies on their etiology, pathophysiology, and treatments remain inconclusive. This narrative review aims to summarise the current state of knowledge regarding the nature of sleep and wake disturbances following TBI, both subjective and objective, spanning all levels of severity and phases post-injury. A second goal is to outline the various causes of post-TBI sleep-wake disturbances. Globally, although sleep-wake complaints are reported in all studies and across all levels of severity, consensus regarding the objective nature of these disturbances is not unanimous and varies widely across studies. In order to optimise recovery in TBI survivors, further studies are required to shed light on the complexity and heterogeneity of post-TBI sleep and wake disturbances, and to fully grasp the best timing and approach for intervention. PMID:25110283

  15. Pathophysiology and Treatment of Severe Traumatic Brain Injuries in Children.

    PubMed

    Allen, Kimberly A

    2016-02-01

    Traumatic brain injuries (TBIs) in children are a major cause of morbidity and mortality worldwide. Severe TBIs account for 15,000 admissions annually and a mortality rate of 24% in children in the United States. The purpose of this article is to explore pathophysiologic events, examine monitoring techniques, and explain current treatment modalities and nursing care related to caring for children with severe TBI. The primary injury of a TBI is because of direct trauma from an external force, a penetrating object, blast waves, or a jolt to the head. Secondary injury occurs because of alterations in cerebral blood flow, and the development of cerebral edema leads to necrotic and apoptotic cellular death after TBI. Monitoring focuses on intracranial pressure, cerebral oxygenation, cerebral edema, and cerebrovascular injuries. If abnormalities are identified, treatments are available to manage the negative effects caused to the cerebral tissue. The mainstay treatments are hyperosmolar therapy; temperature control; cerebrospinal fluid drainage; barbiturate therapy; decompressive craniectomy; analgesia, sedation, and neuromuscular blockade; and antiseizure prophylaxis.

  16. A model for traumatic brain injury using laser induced shockwaves

    NASA Astrophysics Data System (ADS)

    Selfridge, A.; Preece, D.; Gomez, V.; Shi, L. Z.; Berns, M. W.

    2015-08-01

    Traumatic brain injury (TBI) represents a major treatment challenge in both civilian and military medicine; on the cellular level, its mechanisms are poorly understood. As a method to study the dysfunctional repair mechanisms following injury, laser induced shock waves (LIS) are a useful way to create highly precise, well characterized mechanical forces. We present a simple model for TBI using laser induced shock waves as a model for damage. Our objective is to develop an understanding of the processes responsible for neuronal death, the ways in which we can manipulate these processes to improve cell survival and repair, and the importance of these processes at different levels of biological organization. The physics of shock wave creation has been modeled and can be used to calculate forces acting on individual neurons. By ensuring that the impulse is in the same regime as that occurring in practical TBI, the LIS model can ensure that in vitro conditions and damage are similar to those experienced in TBI. This model will allow for the study of the biochemical response of neurons to mechanical stresses, and can be combined with microfluidic systems for cell growth in order to better isolate areas of damage.

  17. Tracheal Decannulation Protocol in Patients Affected by Traumatic Brain Injury

    PubMed Central

    Zanata, Isabel de Lima; Santos, Rosane Sampaio; Hirata, Gisela Carmona

    2014-01-01

    Introduction The frequency of tracheostomy in patients with traumatic brain injury (TBI) contrasts with the lack of objective criteria for its management. The study arose from the need for a protocol in the decision to remove the tracheal tube. Objective To evaluate the applicability of a protocol for tracheal decannulation. Methods A prospective study with 20 patients, ranging between 21 and 85 years of age (average 33.55), 4 of whom were women (20%) and 16 were men (80%). All patients had been diagnosed by a neurologist as having TBI, and the anatomical region of the lesion was known. Patients were evaluated following criteria for tracheal decannulation through a clinical evaluation protocol developed by the authors. Results Decannulation was performed in 12 (60%) patients. Fourteen (70%) had a score greater than 8 on the Glasgow Coma Scale and only 2 (14%) of these were not able to undergo decannulation. Twelve (60%) patients maintained the breathing pattern with occlusion of the tube and were successfully decannulated. Of the 20 patients evaluated, 11 (55%) showed no signs suggestive of tracheal aspiration, and of these, 9 (82%) began training on occlusion of the cannula. The protocol was relevant to establish the beginning of the decannulation process. The clinical assessment should focus on the patient's condition to achieve early tracheal decannulation. Conclusion This study allowed, with the protocol, to establish six criteria for tracheal decannulation: level of consciousness, respiration, tracheal secretion, phonation, swallowing, and coughing. PMID:25992074

  18. Impairments in social cognition following severe traumatic brain injury.

    PubMed

    McDonald, Skye

    2013-03-01

    Severe traumatic brain injury (TBI) leads to physical, neuropsychological, and emotional deficits that interfere with the individual’s capacity to return to his or her former lifestyle. This review focuses on social cognition, that is, the capacity to attend to, recognize and interpret interpersonal cues that guide social behavior. Social cognition entails ‘‘hot’’ processes, that is, emotion perception and emotional empathy and ‘‘cold’’ processes, that is, the ability to infer the beliefs, feelings, and intentions of others (theory of mind: ToM) to see their point of view (cognitive empathy) and what they mean when communicating (pragmatic inference). This review critically examines research attesting to deficits in each of these domains and also examines evidence for theorized mechanisms including specific neural networks, the role of simulation, and non-social cognition. Current research is hampered by small, heterogeneous samples and the inherent complexity of TBI pathology. Nevertheless, there is evidence that facets of social cognition are impaired in this population. New assessment tools to measure social cognition following TBI are required that predict everyday social functioning. In addition, research into remediation needs to be guided by the growing empirical base for understanding social cognition that may yet reveal how deficits dissociate following TBI. PMID:23351330

  19. The characteristics of chronic central pain after traumatic brain injury.

    PubMed

    Ofek, Hadas; Defrin, Ruth

    2007-10-01

    Central pain following traumatic brain injury (TBI) has not been studied in depth. Our purpose was to conduct a systematic study of patients with TBI suffering from chronic central pain, and to describe the characteristics of the central pain. Groups were TBI patients with (TBIP) and without central pain (TBINP) and healthy controls. TBI patients with other pain mechanisms were excluded from the study. Participants underwent quantitative somatosensory testing in the painful and pain-free body regions. Thresholds for warmth, cold, heat-pain, touch and graphesthesia were measured and pathologically evoked pain (allodynia, hyperpathia and wind-up pain) evaluated. Chronic pain was mapped and characterized. Chronic pain developed at a relatively late onset (6.6+/-9 months) was almost exclusively unilateral and reported as pricking, throbbing and burning. Although both TBIP and TBINP exhibited a significant reduction in thermal and tactile sensations compared to controls, thermal sensations in the painful regions of TBIP were significantly more impaired than pain-free regions in the same patients (p<0.01) and in TBINP (p<0.01). Painful regions also exhibited very high rates of allodynia, hyperpathia and exaggerated wind-up. The characteristics of the chronic pain resembled those of other central pain patients although TBIP displayed several unique features. The sensory profile indicated that damage to the pain and temperature systems is a necessary but not sufficient condition for the development of chronic central pain following TBI. Neuronal hyperexcitability may be a contributing factor to the chronic pain.

  20. Health Care Costs 1 Year After Pediatric Traumatic Brain Injury

    PubMed Central

    Rivara, Frederick P.; Vavilala, Monica S.

    2015-01-01

    Objectives. This study sought to estimate total health care costs for mild, moderate, and severe pediatric traumatic brain injury (TBI) and to compare individual- and population-level costs across levels of TBI severity. Methods. Using 2007 to 2010 MarketScan Commercial Claims and Encounters data, we estimated total quarterly health care costs 1 year after TBI among enrollees (aged < 18 years). We compared costs across levels of TBI severity using generalized linear models. Results. Mild TBI accounted for 96.6% of the 319 103 enrollees with TBI; moderate and severe TBI accounted for 1.7% and 1.6%, respectively. Adjusted individual health care costs for moderate and severe TBI were significantly higher than mild TBI in the year after injury (P < .01). At the population level, moderate and severe TBI costs were 88% and 75% less than mild TBI, respectively. Conclusions. Individually, moderate and severe TBI initially generated costs that were markedly higher than those of mild TBI. At the population level, costs following mild TBI far exceeded those of more severe cases, a result of the extremely high population burden of mild TBI. PMID:26270293

  1. Paediatric sports-related mild traumatic brain injury

    PubMed Central

    Keightley, Michelle; Duggan, Catrin Theresa; Reed, Nick; McAuliffe, Jim; Taha, Tim; Faught, Brent; McPherson, Moira; Baker, Joseph; Montelpare, William

    2009-01-01

    Mild traumatic brain injury (mTBI) is a common but relatively understudied childhood injury that can impact cognitive functioning and development. The present report describes a case study of a 14-year-old boy who sustained two consecutive sports-related mTBIs within a 24 h period. Neurocognitive functioning at 2, 6, 8, 55 and 225 days after injury is compared to baseline prior to injury assessment on the same measures. Results from Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT), Conner Continuous Performance Test 2 (CPT-II) and the Attention Network Test (ANT) revealed decreased performance in attention, visual memory functioning and impulsivity, with some measures still not returning to baseline at 225 days post injury. The results are discussed with respect to return to normal activities at 4 days post injury. This case study highlights the need for increased research regarding the clinical management of mTBI in the paediatric population, particularly the potential deleterious effects of cumulative injuries. PMID:21686913

  2. Traumatic Brain Injury – Modeling Neuropsychiatric Symptoms in Rodents

    PubMed Central

    Malkesman, Oz; Tucker, Laura B.; Ozl, Jessica; McCabe, Joseph T.

    2013-01-01

    Each year in the US, ∼1.5 million people sustain a traumatic brain injury (TBI). Victims of TBI can suffer from chronic post-TBI symptoms, such as sensory and motor deficits, cognitive impairments including problems with memory, learning, and attention, and neuropsychiatric symptoms such as depression, anxiety, irritability, aggression, and suicidal rumination. Although partially associated with the site and severity of injury, the biological mechanisms associated with many of these symptoms – and why some patients experience differing assortments of persistent maladies – are largely unknown. The use of animal models is a promising strategy for elucidation of the mechanisms of impairment and treatment, and learning, memory, sensory, and motor tests have widespread utility in rodent models of TBI and psychopharmacology. Comparatively, behavioral tests for the evaluation of neuropsychiatric symptomatology are rarely employed in animal models of TBI and, as determined in this review, the results have been inconsistent. Animal behavioral studies contribute to the understanding of the biological mechanisms by which TBI is associated with neurobehavioral symptoms and offer a powerful means for pre-clinical treatment validation. Therefore, further exploration of the utility of animal behavioral tests for the study of injury mechanisms and therapeutic strategies for the alleviation of emotional symptoms are relevant and essential. PMID:24109476

  3. Therapeutic Hypothermia in Stroke and Traumatic Brain Injury

    PubMed Central

    Faridar, Alireza; Bershad, Eric M.; Emiru, Tenbit; Iaizzo, Paul A.; Suarez, Jose I.; Divani, Afshin A.

    2011-01-01

    Therapeutic hypothermia (TH) is considered to improve survival with favorable neurological outcome in the case of global cerebral ischemia after cardiac arrest and perinatal asphyxia. The efficacy of hypothermia in acute ischemic stroke (AIS) and traumatic brain injury (TBI), however, is not well studied. Induction of TH typically requires a multimodal approach, including the use of both pharmacological agents and physical techniques. To date, clinical outcomes for patients with either AIS or TBI who received TH have yielded conflicting results; thus, no adequate therapeutic consensus has been reached. Nevertheless, it seems that by determining optimal TH parameters and also appropriate applications, cooling therapy still has the potential to become a valuable neuroprotective intervention. Among the various methods for hypothermia induction, intravascular cooling (IVC) may have the most promise in the awake patient in terms of clinical outcomes. Currently, the IVC method has the capability of more rapid target temperature attainment and more precise control of temperature. However, this technique requires expertise in endovascular surgery that can preclude its application in the field and/or in most emergency settings. It is very likely that combining neuroprotective strategies will yield better outcomes than utilizing a single approach. PMID:22207862

  4. Pain Catastrophizing Correlates with Early Mild Traumatic Brain Injury Outcome.

    PubMed

    Chaput, Geneviève; Lajoie, Susanne P; Naismith, Laura M; Lavigne, Gilles

    2016-01-01

    Background. Identifying which patients are most likely to be at risk of chronic pain and other postconcussion symptoms following mild traumatic brain injury (MTBI) is a difficult clinical challenge. Objectives. To examine the relationship between pain catastrophizing, defined as the exaggerated negative appraisal of a pain experience, and early MTBI outcome. Methods. This cross-sectional design included 58 patients diagnosed with a MTBI. In addition to medical chart review, postconcussion symptoms were assessed by self-report at 1 month (Time 1) and 8 weeks (Time 2) after MTBI. Pain severity, psychological distress, level of functionality, and pain catastrophizing were measured by self-report at Time 2. Results. The pain catastrophizing subscales of rumination, magnification, and helplessness were significantly correlated with pain severity (r = .31 to .44), number of postconcussion symptoms reported (r = .35 to .45), psychological distress (r = .57 to .67), and level of functionality (r = -.43 to -.29). Pain catastrophizing scores were significantly higher for patients deemed to be at high risk of postconcussion syndrome (6 or more symptoms reported at both Time 1 and Time 2). Conclusions. Higher levels of pain catastrophizing were related to adverse early MTBI outcomes. The early detection of pain catastrophizing may facilitate goal-oriented interventions to prevent or minimize the development of chronic pain and other postconcussion symptoms. PMID:27445604

  5. Substance P immunoreactivity increases following human traumatic brain injury.

    PubMed

    Zacest, Andrew C; Vink, Robert; Manavis, Jim; Sarvestani, Ghafar T; Blumbergs, Peter C

    2010-01-01

    Recent experimental evidence suggests that neuropeptides, and in particular substance P (SP), are released following traumatic brain injury (TBI) and may play a significant role in the aetiology of cerebral edema and increased intracranial pressure. Whether SP may play a similar role in clinical TBI remains unknown and was investigated in the current study. Archival post-mortem material was selected from patients who had sustained TBI, had died and had undergone post-mortem and detailed neuropathological examination (n = 13). A second cohort of patients who had died, but who showed no neuropathological abnormality (n = 10), served as case controls. Changes in SP immunoreactivity were examined in the cerebral cortex directly beneath the subdural haematoma in 7 TBI cases and in proximity to contusions in the other 6 cases. Increased SP perivascular immunoreactivity was observed after TBI in 10/13 cases, cortical neurones in 12/13 and astrocytes in 10/13 cases. Perivascular axonal injury was observed by amyloid precursor protein (APP) immunoreactivity in 6/13 TBI cases. Co-localization of SP and APP in a small subset of perivascular fibres suggests perivascular axonal injury could be a mechanism of release of this neuropeptide. The abundance of SP fibres around the human cerebral microvasculature, particularly post capillary venules, together with the changes observed following TBI in perivascular axons, cortical neurones and astrocytes suggest a potentially important role for substance P in neurogenic inflammation following human TBI. PMID:19812951

  6. Social reintegration of traumatic brain-injured: the French experience.

    PubMed

    Truelle, J-L; Wild, K Von; Onillon, M; Montreuil, M

    2010-01-01

    Traumatic Brain Injury (TBI) may lead to specific handicap, often hidden, mainly due to cognitive and behavioural sequelae. Social re-entry is a long-term, fluctuant and precarious process. The French experience will be illustrated by 6 initiatives answering to 6 challenges to do with TBI specificities:1. bridging the gap, between initial rehabilitation and community re-entry, via transitional units dealing with assessment, retraining, social/vocational orientation and follow-up. Today, there are 30 such units based on multidisciplinary teams.2. assessing recovery by TBI-specific and validated evaluation tools: EBIS holistic document, BNI Screening of higher cerebral functions, Glasgow outcome extended, and QOLIBRI, a TBI-specific quality of life tool.3. promoting specific re-entry programmes founded on limited medication, ecological neuro-psychological rehabilitation, exchange groups and workshops, violence prevention, continuity of care, environmental structuration, and "resocialisation".4. taking into account the "head injured family"5. facilitating recovery after sports-related concussion6. facing medico-legal consequences and compensation: In that perspective, we developed guidelines for TBI-specific expert appraisal, including mandatory neuro-psychological assessment, family interview and an annual forum gathering lawyers and health professionals. PMID:22028740

  7. Mild pediatric traumatic brain injury: a cohort study.

    PubMed

    Fay, G C; Jaffe, K M; Polissar, N L; Liao, S; Martin, K M; Shurtleff, H A; Rivara, J M; Winn, H R

    1993-09-01

    Using a prospective, cohort design, we investigated whether children with mild traumatic brain injury (TBI) differed from individually matched controls on measures of intellectual, neuropsychological, academic, and "real world" functioning. Subjects included children between the ages of 6 and 15 years who sustained mild, moderate, and severe closed head injuries and were consecutively identified on presentation to the emergency departments of two regional, university medical centers. One hundred twenty-nine children were eligible for enrollment. Seventeen refused enrollment. Fifty-nine of the 112 enrolled children were classified as mildly injured. Six of these children dropped out, leaving 53 mildly injured cases for analysis. Individually matched controls from the classroom of the injured cases were identified based on age, gender, and premorbid academic achievement and behavior. Assessment measures included standardized intellectual, neuropsychological, and academic measures. Also, parent and teacher questionnaires, measuring social, educational, domestic, and community living skills were used. Among 51 outcome variables only five were significantly associated with injury at initial or 1-year testing after adjusting for multiple comparisons. However, these five associations were either very weak or implausible. Results from this study suggest that mild TBI produces virtually no clinically significant long-term deficits in intellectual, neuropsychological, academic, or "real world" functioning. PMID:8379832

  8. Assessment of impulsivity after moderate to severe traumatic brain injury.

    PubMed

    Rochat, Lucien; Beni, Catia; Billieux, Joël; Azouvi, Philippe; Annoni, Jean-Marie; Van der Linden, Martial

    2010-10-01

    The aim of the study was to develop and validate a short questionnaire assessing four dimensions of impulsivity (urgency, lack of premeditation, lack of perseverance, sensation seeking) in patients with traumatic brain injury (TBI). To this end, 82 patients with TBI and their caregivers completed a short questionnaire adapted from the UPPS Impulsive Behavior Scale designed to assess impulsivity changes after TBI. Confirmatory factor analyses (CFAs) performed on the version of the scale completed by the relatives revealed that a hierarchical model holding that lack of premeditation and lack of perseverance are facets of a higher order construct (lack of conscientiousness), with urgency and sensation seeking as separate correlated factors, fit the data best. Urgency, lack of premeditation, and lack of perseverance increased after the TBI, whereas sensation seeking decreased. CFA failed to reveal a satisfactory model in the version of the scale completed by the patients. The psychological processes related to these impulsivity changes and the discrepancy observed between self-report and informant-report are discussed. This short questionnaire opens up interesting prospects for better comprehension and assessment of behavioural symptoms of TBI. PMID:20635306

  9. Narrative skills following traumatic brain injury in children and adults.

    PubMed

    Biddle, K R; McCabe, A; Bliss, L S

    1996-01-01

    Personal narratives serve an important function in virtually all societies (Peterson & McCabe, 1991). Through narratives individuals make sense of their experiences and represent themselves to others (Bruner, 1990). The ability to produce narratives has been linked to academic success (Feagans, 1982). Persons who have sustained a traumatic brain injury (TBI) are at risk for impaired narrative ability (Dennis, 1991). However, a paucity of information exists on the discourse abilities of persons with TBI. This is partly due to a lack of reliable tools with which to assess narrative discourse. The present study utilized dependency analysis (Deese, 1984) to document and describe the narrative discourse impairments of children and adults with TBI. Ten children (mean age 12;0) and 10 adults (mean age 35;2) were compared with matched controls. Dependency analysis reliably differentiated the discourse of the individuals with TBI from their controls. Individuals with TBI were significantly more dysfluent than their matched controls. Furthermore, their performance on the narrative task revealed a striking listener burden.

  10. Systematic Review of Traumatic Brain Injury Animal Models.

    PubMed

    Phipps, Helen W

    2016-01-01

    The goals of this chapter are to provide an introduction into the variety of animal models available for studying traumatic brain injury (TBI) and to provide a concise systematic review of the general materials and methods involved in each model. Materials and methods were obtained from a literature search of relevant peer-reviewed articles. Strengths and weaknesses of each animal choice were presented to include relative cost, anatomical and physiological features, and mechanism of injury desired. Further, a variety of homologous, isomorphic/induced, and predictive animal models were defined, described, and compared with respect to their relative ease of use, characteristics, range, adjustability (e.g., amplitude, duration, mass/size, velocity, and pressure), and rough order of magnitude cost. Just as the primary mechanism of action of TBI is limitless, so are the animal models available to study TBI. With such a wide variety of available animals, types of injury models, along with the research needs, there exists no single "gold standard" model of TBI rendering cross-comparison of data extremely difficult. Therefore, this chapter reflects a representative sampling of the TBI animal models available and is not an exhaustive comparison of every possible model and associated parameters. Throughout this chapter, special considerations for animal choice and TBI animal model classification are discussed. Criteria central to choosing appropriate animal models of TBI include ethics, funding, complexity (ease of use, safety, and controlled access requirements), type of model, model characteristics, and range of control (scope). PMID:27604713

  11. Multi-modal MRI of mild traumatic brain injury

    PubMed Central

    Narayana, Ponnada A.; Yu, Xintian; Hasan, Khader M.; Wilde, Elisabeth A.; Levin, Harvey S.; Hunter, Jill V.; Miller, Emmy R.; Patel, Vipul Kumar S.; Robertson, Claudia S.; McCarthy, James J.

    2014-01-01

    Multi-modal magnetic resonance imaging (MRI) that included high resolution structural imaging, diffusion tensor imaging (DTI), magnetization transfer ratio (MTR) imaging, and magnetic resonance spectroscopic imaging (MRSI) were performed in mild traumatic brain injury (mTBI) patients with negative computed tomographic scans and in an orthopedic-injured (OI) group without concomitant injury to the brain. The OI group served as a comparison group for mTBI. MRI scans were performed both in the acute phase of injury (~24 h) and at follow-up (~90 days). DTI data was analyzed using tract based spatial statistics (TBSS). Global and regional atrophies were calculated using tensor-based morphometry (TBM). MTR values were calculated using the standard method. MRSI was analyzed using LC Model. At the initial scan, the mean diffusivity (MD) was significantly higher in the mTBI cohort relative to the comparison group in several white matter (WM) regions that included internal capsule, external capsule, superior corona radiata, anterior corona radiata, posterior corona radiata, inferior fronto-occipital fasciculus, inferior longitudinal fasciculus, forceps major and forceps minor of the corpus callosum, superior longitudinal fasciculus, and corticospinal tract in the right hemisphere. TBSS analysis failed to detect significant differences in any DTI measures between the initial and follow-up scans either in the mTBI or OI group. No significant differences were found in MRSI, MTR or morphometry between the mTBI and OI cohorts either at the initial or follow-up scans with or without family wise error (FWE) correction. Our study suggests that a number of WM tracts are affected in mTBI in the acute phase of injury and that these changes disappear by 90 days. This study also suggests that none of the MRI-modalities used in this study, with the exception of DTI, is sensitive in detecting changes in the acute phase of mTBI. PMID:25610770

  12. Genomic responses in rat cerebral cortex after traumatic brain injury

    PubMed Central

    von Gertten, Christina; Morales, Amilcar Flores; Holmin, Staffan; Mathiesen, Tiit; Nordqvist, Ann-Christin Sandberg

    2005-01-01

    Background Traumatic brain injury (TBI) initiates a complex sequence of destructive and neuroprotective cellular responses. The initial mechanical injury is followed by an extended time period of secondary brain damage. Due to the complicated pathological picture a better understanding of the molecular events occurring during this secondary phase of injury is needed. This study was aimed at analysing gene expression patterns following cerebral cortical contusion in rat using high throughput microarray technology with the goal of identifying genes involved in an early and in a more delayed phase of trauma, as genomic responses behind secondary mechanisms likely are time-dependent. Results Among the upregulated genes 1 day post injury, were transcription factors and genes involved in metabolism, e.g. STAT-3, C/EBP-δ and cytochrome p450. At 4 days post injury we observed increased gene expression of inflammatory factors, proteases and their inhibitors, like cathepsins, α-2-macroglobulin and C1q. Notably, genes with biological function clustered to immune response were significantly upregulated 4 days after injury, which was not found following 1 day. Osteopontin and one of its receptors, CD-44, were both upregulated showing a local mRNA- and immunoreactivity pattern in and around the injury site. Fewer genes had decreased expression both 1 and 4 days post injury and included genes implicated in transport, metabolism, signalling, and extra cellular matrix formation, e.g. vitronectin, neuroserpin and angiotensinogen. Conclusion The different patterns of gene expression, with little overlap in genes, 1 and 4 days post injury showed time dependence in genomic responses to trauma. An early induction of factors involved in transcription could lead to the later inflammatory response with strongly upregulated CD-44 and osteopontin expression. An increased knowledge of genes regulating the pathological mechanisms in trauma will help to find future treatment targets. Since

  13. Effect of cocaine use on outcomes in traumatic brain injury

    PubMed Central

    Yeung, Jacky T; Williams, Jessica; Bowling, William M

    2013-01-01

    Context: Animal and molecular studies have shown that cocaine exerts a neuroprotective effect against cerebral ischemia. Aims: To determine if the presence of cocaine metabolites on admission following traumatic brain injury (TBI) is associated with better outcomes. Settings and Design: Level-1 trauma center, retrospective cohort. Materials and Methods: After obtaining Institutional Review Board (IRB) approval, the trauma registry was searched from 2006 to 2009 for all patients aged 15-55 years with blunt head trauma and non-head AIS <3. Exclusion criteria were pre-existing brain pathology and death within 30 min of admission. The primary outcome was in-hospital mortality; secondary outcomes were hospital length of stay (LOS), and Glasgow Outcome Score (GOS). Statistical Analysis: Logistic regression was used to determine the independent effect of cocaine on mortality. Hospital LOS was compared with multiple linear regression. Results: A total of 741 patients met criteria and had drug screens. The screened versus unscreened groups were similar. Cocaine positive patients were predominantly African-American (46% vs. 21%, P < 0.0001), older (40 years vs. 30 years, P < 0.0001), and had ethanol present more often (50.7% vs. 37.8%, P = 0.01). There were no differences in mortality (cocaine-positive 1.4% vs. cocaine-negative 2.7%, P = 0.6) on both univariate and multivariate analysis. Conclusions: Positive cocaine screening was not associated with mortality in TBI. An effect may not have been detected because of the low mortality rate. LOS is affected by many factors unrelated to the injury and may not be a good surrogate for recovery. Similarly, GOS may be too coarse a measure to identify a benefit. PMID:23960376

  14. Multi-modal MRI of mild traumatic brain injury.

    PubMed

    Narayana, Ponnada A; Yu, Xintian; Hasan, Khader M; Wilde, Elisabeth A; Levin, Harvey S; Hunter, Jill V; Miller, Emmy R; Patel, Vipul Kumar S; Robertson, Claudia S; McCarthy, James J

    2015-01-01

    Multi-modal magnetic resonance imaging (MRI) that included high resolution structural imaging, diffusion tensor imaging (DTI), magnetization transfer ratio (MTR) imaging, and magnetic resonance spectroscopic imaging (MRSI) were performed in mild traumatic brain injury (mTBI) patients with negative computed tomographic scans and in an orthopedic-injured (OI) group without concomitant injury to the brain. The OI group served as a comparison group for mTBI. MRI scans were performed both in the acute phase of injury (~24 h) and at follow-up (~90 days). DTI data was analyzed using tract based spatial statistics (TBSS). Global and regional atrophies were calculated using tensor-based morphometry (TBM). MTR values were calculated using the standard method. MRSI was analyzed using LC Model. At the initial scan, the mean diffusivity (MD) was significantly higher in the mTBI cohort relative to the comparison group in several white matter (WM) regions that included internal capsule, external capsule, superior corona radiata, anterior corona radiata, posterior corona radiata, inferior fronto-occipital fasciculus, inferior longitudinal fasciculus, forceps major and forceps minor of the corpus callosum, superior longitudinal fasciculus, and corticospinal tract in the right hemisphere. TBSS analysis failed to detect significant differences in any DTI measures between the initial and follow-up scans either in the mTBI or OI group. No significant differences were found in MRSI, MTR or morphometry between the mTBI and OI cohorts either at the initial or follow-up scans with or without family wise error (FWE) correction. Our study suggests that a number of WM tracts are affected in mTBI in the acute phase of injury and that these changes disappear by 90 days. This study also suggests that none of the MRI-modalities used in this study, with the exception of DTI, is sensitive in detecting changes in the acute phase of mTBI.

  15. Neuroprotective efficacy of a proneurogenic compound after traumatic brain injury.

    PubMed

    Blaya, Meghan O; Bramlett, Helen M; Naidoo, Jacinth; Pieper, Andrew A; Dietrich, W Dalton

    2014-03-01

    Traumatic brain injury (TBI) is characterized by histopathological damage and long-term sensorimotor and cognitive dysfunction. Recent studies have reported the discovery of the P7C3 class of aminopropyl carbazole agents with potent neuroprotective properties for both newborn neural precursor cells in the adult hippocampus and mature neurons in other regions of the central nervous system. This study tested, for the first time, whether the highly active P7C3-A20 compound would be neuroprotective, promote hippocampal neurogenesis, and improve functional outcomes after experimental TBI. Sprague-Dawley rats subjected to moderate fluid percussion brain injury were evaluated for quantitative immunohistochemical and behavioral changes after trauma. P7C3-A20 (10 mg/kg) or vehicle was initiated intraperitoneally 30 min postsurgery and twice per day every day thereafter for 7 days. Administration of P7C3-A20 significantly reduced overall contusion volume, preserved vulnerable anti-neuronal nuclei (NeuN)-positive pericontusional cortical neurons, and improved sensorimotor function 1 week after trauma. P7C3-A20 treatment also significantly increased both bromodeoxyuridine (BrdU)- and doublecortin (DCX)-positive cells within the subgranular zone of the ipsilateral dentate gyrus 1 week after TBI. Five weeks after TBI, animals treated with P7C3-A20 showed significantly increased BrdU/NeuN double-labeled neurons and improved cognitive function in the Morris water maze, compared to TBI-control animals. These results suggest that P7C3-A20 is neuroprotective and promotes endogenous reparative strategies after TBI. We propose that the chemical scaffold represented by P7C3-A20 provides a basis for optimizing and advancing new pharmacological agents for protecting patients against the early and chronic consequences of TBI. PMID:24070637

  16. Traumatic Brain Injury Upregulates Phosphodiesterase Expression in the Hippocampus.

    PubMed

    Wilson, Nicole M; Titus, David J; Oliva, Anthony A; Furones, Concepcion; Atkins, Coleen M

    2016-01-01

    Traumatic brain injury (TBI) results in significant impairments in hippocampal synaptic plasticity. A molecule critically involved in hippocampal synaptic plasticity, 3',5'-cyclic adenosine monophosphate, is downregulated in the hippocampus after TBI, but the mechanism that underlies this decrease is unknown. To address this question, we determined whether phosphodiesterase (PDE) expression in the hippocampus is altered by TBI. Young adult male Sprague Dawley rats received sham surgery or moderate parasagittal fluid-percussion brain injury. Animals were analyzed by western blotting for changes in PDE expression levels in the hippocampus. We found that PDE1A levels were significantly increased at 30 min, 1 h and 6 h after TBI. PDE4B2 and 4D2 were also significantly increased at 1, 6, and 24 h after TBI. Additionally, phosphorylation of PDE4A was significantly increased at 6 and 24 h after TBI. No significant changes were observed in levels of PDE1B, 1C, 3A, 8A, or 8B between 30 min to 7 days after TBI. To determine the spatial profile of these increases, we used immunohistochemistry and flow cytometry at 24 h after TBI. PDE1A and phospho-PDE4A localized to neuronal cell bodies. PDE4B2 was expressed in neuronal dendrites, microglia and infiltrating CD11b(+) immune cells. PDE4D was predominantly found in microglia and infiltrating CD11b(+) immune cells. To determine if inhibition of PDE4 would improve hippocampal synaptic plasticity deficits after TBI, we treated hippocampal slices with rolipram, a pan-PDE4 inhibitor. Rolipram partially rescued the depression in basal synaptic transmission and converted a decaying form of long-term potentiation (LTP) into long-lasting LTP. Overall, these results identify several possible PDE targets for reducing hippocampal synaptic plasticity deficits and improving cognitive function acutely after TBI. PMID:26903822

  17. Common biochemical defects linkage between post-traumatic stress disorders, mild traumatic brain injury (TBI) and penetrating TBI.

    PubMed

    Prasad, Kedar N; Bondy, Stephen C

    2015-03-01

    Post-traumatic stress disorder (PTSD) is a complex mental disorder with psychological and emotional components, caused by exposure to single or repeated extreme traumatic events found in war, terrorist attacks, natural or man-caused disasters, and by violent personal assaults and accidents. Mild traumatic brain injury (TBI) occurs when the brain is violently rocked back and forth within the skull following a blow to the head or neck as in contact sports, or when in close proximity to a blast pressure wave following detonation of explosives in the battlefield. Penetrating TBI occurs when an object penetrates the skull and damages the brain, and is caused by vehicle crashes, gunshot wound to the head, and exposure to solid fragments in the proximity of explosions, and other combat-related head injuries. Despite clinical studies and improved understanding of the mechanisms of cellular damage, prevention and treatment strategies for patients with PTSD and TBI remain unsatisfactory. To develop an improved plan for treating and impeding progression of PTSD and TBI, it is important to identify underlying biochemical changes that may play key role in the initiation and progression of these disorders. This review identifies three common biochemical events, namely oxidative stress, chronic inflammation and excitotoxicity that participate in the initiation and progression of these conditions. While these features are separately discussed, in many instances, they overlap. This review also addresses the goal of developing novel treatments and drug regimens, aimed at combating this triad of events common to, and underlying, injury to the brain.

  18. Prediction of brain age suggests accelerated atrophy after traumatic brain injury

    PubMed Central

    Cole, James H; Leech, Robert; Sharp, David J

    2015-01-01

    Objective The long-term effects of traumatic brain injury (TBI) can resemble observed in normal ageing, suggesting that TBI may accelerate the ageing process. We investigate this using a neuroimaging model that predicts brain age in healthy individuals and then apply it to TBI patients. We define individuals' differences in chronological and predicted structural "brain age," and test whether TBI produces progressive atrophy and how this relates to cognitive function. Methods A predictive model of normal ageing was defined using machine learning in 1,537 healthy individuals, based on magnetic resonance imaging–derived estimates of gray matter (GM) and white matter (WM). This ageing model was then applied to test 99 TBI patients and 113 healthy controls to estimate brain age. Results The initial model accurately predicted age in healthy individuals (r * 0.92). TBI brains were estimated to be "older," with a mean predicted age difference (PAD) between chronological and estimated brain age of 4.66 years (±10.8) for GM and 5.97 years (±11.22) for WM. This PAD predicted cognitive impairment and correlated strongly with the time since TBI, indicating that brain tissue loss increases throughout the chronic postinjury phase. Interpretation TBI patients' brains were estimated to be older than their chronological age. This discrepancy increases with time since injury, suggesting that TBI accelerates the rate of brain atrophy. This may be an important factor in the increased susceptibility in TBI patients for dementia and other age-associated conditions, motivating further research into the age-like effects of brain injury and other neurological diseases. PMID:25623048

  19. Endogenous Neural Stem/Progenitor Cells Stabilize the Cortical Microenvironment after Traumatic Brain Injury

    PubMed Central

    Dixon, Kirsty J.; Theus, Michelle H.; Nelersa, Claudiu M.; Mier, Jose; Travieso, Lissette G.; Yu, Tzong-Shiue; Kernie, Steven G.

    2015-01-01

    Abstract Although a myriad of pathological responses contribute to traumatic brain injury (TBI), cerebral dysfunction has been closely linked to cell death mechanisms. A number of therapeutic strategies have been studied in an attempt to minimize or ameliorate tissue damage; however, few studies have evaluated the inherent protective capacity of the brain. Endogenous neural stem/progenitor cells (NSPCs) reside in distinct brain regions and have been shown to respond to tissue damage by migrating to regions of injury. Until now, it remained unknown whether these cells have the capacity to promote endogenous repair. We ablated NSPCs in the subventricular zone to examine their contribution to the injury microenvironment after controlled cortical impact (CCI) injury. Studies were performed in transgenic mice expressing the herpes simplex virus thymidine kinase gene under the control of the nestinδ promoter exposed to CCI injury. Two weeks after CCI injury, mice deficient in NSPCs had reduced neuronal survival in the perilesional cortex and fewer Iba-1-positive and glial fibrillary acidic protein-positive glial cells but increased glial hypertrophy at the injury site. These findings suggest that the presence of NSPCs play a supportive role in the cortex to promote neuronal survival and glial cell expansion after TBI injury, which corresponds with improvements in motor function. We conclude that enhancing this endogenous response may have acute protective roles after TBI. PMID:25290253

  20. The Relation of Focal Lesions to Cortical Thickness in Pediatric Traumatic Brain Injury.

    PubMed

    Bigler, Erin D; Zielinski, Brandon A; Goodrich-Hunsaker, Naomi; Black, Garrett M; Huff, B S Trevor; Christiansen, Zachary; Wood, Dawn-Marie; Abildskov, Tracy J; Dennis, Maureen; Taylor, H Gerry; Rubin, Kenneth; Vannatta, Kathryn; Gerhardt, Cynthia A; Stancin, Terry; Yeates, Keith Owen

    2016-10-01

    In a sample of children with traumatic brain injury, this magnetic resonance imaging (MRI)-based investigation examined whether presence of a focal lesion uniquely influenced cortical thickness in any brain region. Specifically, the study explored the relation of cortical thickness to injury severity as measured by Glasgow Coma Scale score and length of stay, along with presence of encephalomalacia, focal white matter lesions or presence of hemosiderin deposition as a marker of shear injury. For comparison, a group of children without head injury but with orthopedic injury of similar age and sex were also examined. Both traumatic brain injury and orthopedic injury children had normally reduced cortical thickness with age, assumed to reflect neuronal pruning. However, the reductions observed within the traumatic brain injury sample were similar to those in the orthopedic injury group, suggesting that in this sample traumatic brain injury, per se, did not uniquely alter cortical thickness in any brain region at the group level. Injury severity in terms of Glasgow Coma Scale or longer length of stay was associated with greater reductions in frontal and occipitoparietal cortical thickness. However, presence of focal lesions were not related to unique changes in cortical thickness despite having a prominent distribution of lesions within frontotemporal regions among children with traumatic brain injury. Because focal lesions were highly heterogeneous, their association with cortical thickness and development appeared to be idiosyncratic, and not associated with group level effects.

  1. Inflammation and white matter degeneration persist for years after a single traumatic brain injury.

    PubMed

    Johnson, Victoria E; Stewart, Janice E; Begbie, Finn D; Trojanowski, John Q; Smith, Douglas H; Stewart, William

    2013-01-01

    A single traumatic brain injury is associated with an increased risk of dementia and, in a proportion of patients surviving a year or more from injury, the development of hallmark Alzheimer's disease-like pathologies. However, the pathological processes linking traumatic brain injury and neurodegenerative disease remain poorly understood. Growing evidence supports a role for neuroinflammation in the development of Alzheimer's disease. In contrast, little is known about the neuroinflammatory response to brain injury and, in particular, its temporal dynamics and any potential role in neurodegeneration. Cases of traumatic brain injury with survivals ranging from 10 h to 47 years post injury (n = 52) and age-matched, uninjured control subjects (n = 44) were selected from the Glasgow Traumatic Brain Injury archive. From these, sections of the corpus callosum and adjacent parasaggital cortex were examined for microglial density and morphology, and for indices of white matter pathology and integrity. With survival of ≥3 months from injury, cases with traumatic brain injury frequently displayed extensive, densely packed, reactive microglia (CR3/43- and/or CD68-immunoreactive), a pathology not seen in control subjects or acutely injured cases. Of particular note, these reactive microglia were present in 28% of cases with survival of >1 year and up to 18 years post-trauma. In cases displaying this inflammatory pathology, evidence of ongoing white matter degradation could also be observed. Moreover, there was a 25% reduction in the corpus callosum thickness with survival >1 year post-injury. These data present striking evidence of persistent inflammation and ongoing white matter degeneration for many years after just a single traumatic brain injury in humans. Future studies to determine whether inflammation occurs in response to or, conversely, promotes white matter degeneration will be important. These findings may provide parallels for studying neurodegenerative disease

  2. Objective Neuropsychological Deficits in Post-Traumatic Stress Disorder and Mild Traumatic Brain Injury: What Remains Beyond Symptom Similarity?

    PubMed Central

    Pineau, Hélène; Marchand, André; Guay, Stéphane

    2014-01-01

    This exploratory study intends to characterize the neuropsychological profile in persons with post-traumatic stress disorder (PTSD) and mild traumatic brain injury (mTBI) using objective measures of cognitive performance. A neuropsychological battery of tests for attention, memory and executive functions was administered to four groups: PTSD (n = 25), mTBI (n = 19), subjects with two formal diagnoses: Post-traumatic Stress Disorder and Mild Traumatic Brain Injury (mTBI/PTSD) (n = 6) and controls (n = 25). Confounding variables, such as medical, developmental or neurological antecedents, were controlled and measures of co-morbid conditions, such as depression and anxiety, were considered. The PTSD and mTBI/PTSD groups reported more anxiety and depressive symptoms. They also presented more cognitive deficits than the mTBI group. Since the two PTSD groups differ in severity of PTSD symptoms but not in severity of depression and anxiety symptoms, the PTSD condition could not be considered as the unique factor affecting the results. The findings underline the importance of controlling for confounding medical and psychological co-morbidities in the evaluation and treatment of PTSD populations, especially when a concomitant mTBI is also suspected. PMID:25469837

  3. Magnetic Micelles for DNA delivery to rat brains after mild traumatic brain injury

    PubMed Central

    Das, Mahasweta; Wang, Chunyan; Bedi, Raminder; Mohapatra, Shyam S.; Mohapatra, Subhra

    2014-01-01

    Traumatic brain injury (TBI) causes significant mortality, long term disability and psychological symptoms. Gene therapy is a promising approach for treatment of different pathological conditions. Here we tested chitosan and polyethyleneimine (PEI)-coated magnetic micelles (CPmag micelles or CPMMs), a potential MRI contrast agent, to deliver a reporter DNA to the brain after mild TBI (mTBI). CPMM - tomato plasmid (ptd) conjugate expressing a red-fluorescent protein (RFP) was administered intranasally immediately after mTBI or sham surgery in male SD rats. Evans blue extravasation following mTBI suggested CPMM-ptd entry into the brain via the compromised blood-brain barrier. Magnetofection increased the concentration of CPMMs in the brain. RFP expression was observed in the brain (cortex and hippocampus), lung and liver 48 hours after mTBI. CPMM did not evoke any inflammatory response by themselves and were excreted from the body. These results indicate the possibility of using intranasally administered CPMM as a theranostic vehicle for mTBI. PMID:24486465

  4. Clinical utility of brain stimulation modalities following traumatic brain injury: current evidence

    PubMed Central

    Li, Shasha; Zaninotto, Ana Luiza; Neville, Iuri Santana; Paiva, Wellingson Silva; Nunn, Danuza; Fregni, Felipe

    2015-01-01

    Traumatic brain injury (TBI) remains the main cause of disability and a major public health problem worldwide. This review focuses on the neurophysiology of TBI, and the rationale and current state of evidence of clinical application of brain stimulation to promote TBI recovery, particularly on consciousness, cognitive function, motor impairments, and psychiatric conditions. We discuss the mechanisms of different brain stimulation techniques including major noninvasive and invasive stimulations. Thus far, most noninvasive brain stimulation interventions have been nontargeted and focused on the chronic phase of recovery after TBI. In the acute stages, there is limited available evidence of the efficacy and safety of brain stimulation to improve functional outcomes. Comparing the studies across different techniques, transcranial direct current stimulation is the intervention that currently has the higher number of properly designed clinical trials, though total number is still small. We recognize the need for larger studies with target neuroplasticity modulation to fully explore the benefits of brain stimulation to effect TBI recovery during different stages of recovery. PMID:26170670

  5. The Changed Brain: Teacher Awareness of Traumatic Brain Injury and Instruction Methods to Enhance Cognitive Processing in Mathematics

    ERIC Educational Resources Information Center

    Stahl, Judith M.

    2008-01-01

    Traumatic brain injury (TBI) has come to subjugate and exert its authority on education as some survivors re-enter the academic arena. A key component of a TBI student's academic success is dependent upon a teacher's awareness of the TBI learner and a willingness to modify curriculum to promote the uniqueness of the changed brain and therefore,…

  6. Disconnection of network hubs and cognitive impairment after traumatic brain injury.

    PubMed

    Fagerholm, Erik D; Hellyer, Peter J; Scott, Gregory; Leech, Robert; Sharp, David J

    2015-06-01

    Traumatic brain injury affects brain connectivity by producing traumatic axonal injury. This disrupts the function of large-scale networks that support cognition. The best way to describe this relationship is unclear, but one elegant approach is to view networks as graphs. Brain regions become nodes in the graph, and white matter tracts the connections. The overall effect of an injury can then be estimated by calculating graph metrics of network structure and function. Here we test which graph metrics best predict the presence of traumatic axonal injury, as well as which are most highly associated with cognitive impairment. A comprehensive range of graph metrics was calculated from structural connectivity measures for 52 patients with traumatic brain injury, 21 of whom had microbleed evidence of traumatic axonal injury, and 25 age-matched controls. White matter connections between 165 grey matter brain regions were defined using tractography, and structural connectivity matrices calculated from skeletonized diffusion tensor imaging data. This technique estimates injury at the centre of tract, but is insensitive to damage at tract edges. Graph metrics were calculated from the resulting connectivity matrices and machine-learning techniques used to select the metrics that best predicted the presence of traumatic brain injury. In addition, we used regularization and variable selection via the elastic net to predict patient behaviour on tests of information processing speed, executive function and associative memory. Support vector machines trained with graph metrics of white matter connectivity matrices from the microbleed group were able to identify patients with a history of traumatic brain injury with 93.4% accuracy, a result robust to different ways of sampling the data. Graph metrics were significantly associated with cognitive performance: information processing speed (R(2) = 0.64), executive function (R(2) = 0.56) and associative memory (R(2) = 0.25). These

  7. Top-cited articles in traumatic brain injury.

    PubMed

    Sharma, Bhanu; Lawrence, David Wyndham

    2014-01-01

    A review of the top-cited articles in a scientific discipline can identify areas of research that are well established and those in need of further development, and may, as a result, inform and direct future research efforts. Our objective was to identify and characterize the top-cited articles in traumatic brain injury (TBI). We used publically available software to identify the 50 TBI articles with the most lifetime citations, and the 50 TBI articles with the highest annual citation rates. A total of 73 articles were included in this review, with 27 of the 50 papers with the highest annual citation rates common to the cohort of 50 articles with the most lifetime citations. All papers were categorized by their primary topic or focus, namely: predictor of outcome, pathology/natural history, treatment, guidelines and consensus statements, epidemiology, assessment measures, or experimental model of TBI. The mean year of publication of the articles with the most lifetime citations and highest annual citation rates was 1990 ± 14.9 years and 2003 ± 6.7 years, respectively. The 50 articles with the most lifetime citations typically studied predictors of outcome (34.0%, 17/50) and were specific to severe TBI (38.0%, 19/50). In contrast, the most common subject of papers with the highest annual citation rates was treatment of brain injury (22.0%, 11/50), and these papers most frequently investigated mild TBI (36.0%, 18/50). These findings suggest an intensified focus on mild TBI, which is perhaps a response to the dedicated attention these injuries are currently receiving in the context of sports and war, and because of their increasing incidence in developing nations. Our findings also indicate increased focus on treatment of TBI, possibly due to the limited efficacy of current interventions for brain injury. This review provides a cross-sectional summary of some of the most influential articles in TBI, and a bibliometric examination of the current status of

  8. Gender differences in self reported long term outcomes following moderate to severe traumatic brain injury

    PubMed Central

    2010-01-01

    Background The majority of research on health outcomes after a traumatic brain injury is focused on male participants. Information examining gender differences in health outcomes post traumatic brain injury is limited. The purpose of this study was to investigate gender differences in symptoms reported after a traumatic brain injury and to examine the degree to which these symptoms are problematic in daily functioning. Methods This is a secondary data analysis of a retrospective cohort study of 306 individuals who sustained a moderate to severe traumatic brain injury 8 to 24 years ago. Data were collected using the Problem Checklist (PCL) from the Head Injury Family Interview (HIFI). Using Bonferroni correction, group differences between women and men were explored using Chi-square and Wilcoxon analysis. Results Chi-square analysis by gender revealed that significantly more men reported difficulty setting realistic goals and restlessness whereas significantly more women reported headaches, dizziness and loss of confidence. Wilcoxon analysis by gender revealed that men reported sensitivity to noise and sleep disturbances as significantly more problematic than women, whereas for women, lack of initiative and needing supervision were significantly more problematic in daily functioning. Conclusion This study provides insight into gender differences on outcomes after traumatic brain injury. There are significant differences between problems reported by men compared to women. This insight may facilitate health service planners and clinicians when developing programs for individuals with brain injury. PMID:21029463

  9. Eye Tracking Detects Disconjugate Eye Movements Associated with Structural Traumatic Brain Injury and Concussion

    PubMed Central

    Ritlop, Robert; Reyes, Marleen; Nehrbass, Elena; Li, Meng; Lamm, Elizabeth; Schneider, Julia; Shimunov, David; Sava, Maria; Kolecki, Radek; Burris, Paige; Altomare, Lindsey; Mehmood, Talha; Smith, Theodore; Huang, Jason H.; McStay, Christopher; Todd, S. Rob; Qian, Meng; Kondziolka, Douglas; Wall, Stephen; Huang, Paul

    2015-01-01

    Abstract Disconjugate eye movements have been associated with traumatic brain injury since ancient times. Ocular motility dysfunction may be present in up to 90% of patients with concussion or blast injury. We developed an algorithm for eye tracking in which the Cartesian coordinates of the right and left pupils are tracked over 200 sec and compared to each other as a subject watches a short film clip moving inside an aperture on a computer screen. We prospectively eye tracked 64 normal healthy noninjured control subjects and compared findings to 75 trauma subjects with either a positive head computed tomography (CT) scan (n=13), negative head CT (n=39), or nonhead injury (n=23) to determine whether eye tracking would reveal the disconjugate gaze associated with both structural brain injury and concussion. Tracking metrics were then correlated to the clinical concussion measure Sport Concussion Assessment Tool 3 (SCAT3) in trauma patients. Five out of five measures of horizontal disconjugacy were increased in positive and negative head CT patients relative to noninjured control subjects. Only one of five vertical disconjugacy measures was significantly increased in brain-injured patients relative to controls. Linear regression analysis of all 75 trauma patients demonstrated that three metrics for horizontal disconjugacy negatively correlated with SCAT3 symptom severity score and positively correlated with total Standardized Assessment of Concussion score. Abnormal eye-tracking metrics improved over time toward baseline in brain-injured subjects observed in follow-up. Eye tracking may help quantify the severity of ocular motility disruption associated with concussion and structural brain injury. PMID:25582436

  10. The Impact of Previous Traumatic Brain Injury on Health and Functioning: A TRACK-TBI Study

    PubMed Central

    Spielman, Lisa; Singh, Ayushi; Gordon, Wayne A.; Lingsma, Hester F.; Maas, Andrew I.R.; Manley, Geoffrey T.; Mukherjee, Pratik; Okonkwo, David O.; Puccio, Ava M.; Schnyer, David M.; Valadka, Alex B.; Yue, John K.; Yuh, Esther L.; Casey, and the TRACK-TBI Investigators including: Scott S.; Cooper, Shelly R.; Cheong, Maxwell; Hricik, Allison J.; Knight, Emily E.; Menon, David K.; Morabito, Diane J.; Pacheco, Jennifer L.; Sinha, Tuhin K.; Vassar, Mary J.

    2013-01-01

    Abstract The idea that multiple traumatic brain injury (TBI) can have a cumulative detrimental effect on functioning is widely accepted. Most research supporting this idea comes from athlete samples, and it is not known whether remote history of previous TBI affects functioning after subsequent TBI in community-based samples. This study investigates whether a previous history of TBI with loss of consciousness (LOC) is associated with worse health and functioning in a sample of individuals who require emergency department care for current TBI. Twenty-three percent of the 586 individuals with current TBI in the Transforming Research and Clinical Knowledge in Traumatic Brain Injury study reported having sustained a previous TBI with LOC. Individuals with previous TBI were more likely to be unemployed (χ2=17.86; p=0.000), report a variety of chronic medical and psychiatric conditions (4.75≤χ2≥24.16; p<0.05), and report substance use (16.35≤χ2≥27.57; p<0.01) before the acute injury, compared to those with no previous TBI history. Those with a previous TBI had less-severe acute injuries, but experienced worse outcomes at 6-month follow-up. Results of a series of regression analyses controlling for demographics and acute injury severity indicated that individuals with previous TBI reported more mood symptoms, more postconcussive symptoms, lower life satisfaction, and had slower processing speed and poorer verbal learning, compared to those with no previous TBI history. These findings suggest that history of TBI with LOC may have important implications for health and psychological functioning after TBI in community-based samples. PMID:23924069

  11. Increased brain activation during working memory processing after pediatric mild traumatic brain injury (mTBI)

    PubMed Central

    Westfall, Daniel R.; West, John D.; Bailey, Jessica N.; Arnold, Todd W.; Kersey, Patrick A.; Saykin, Andrew J.; McDonald, Brenna C.

    2016-01-01

    Purpose The neural substrate of post-concussive symptoms following the initial injury period after mild traumatic brain injury (mTBI) in pediatric populations remains poorly elucidated. This study examined neuropsychological, behavioral, and brain functioning in adolescents post-mTBI to assess whether persistent differences were detectable up to a year post-injury. Methods Nineteen adolescents (mean age 14.7 years) who experienced mTBI 3–12 months previously (mean 7.5 months) and 19 matched healthy controls (mean age 14.0 years) completed neuropsychological testing and an fMRI auditory-verbal N-back working memory task. Parents completed behavioral ratings. Results No between-group differences were found for cognition, behavior, or N-back task performance, though the expected decreased accuracy and increased reaction time as task difficulty increased were apparent. However, the mTBI group showed significantly greater brain activation than controls during the most difficult working memory task condition. Conclusion Greater working memory task-related activation was found in adolescents up to one year post-mTBI relative to controls, potentially indicating compensatory activation to support normal task performance. Differences in brain activation in the mTBI group so long after injury may indicate residual alterations in brain function much later than would be expected based on the typical pattern of natural recovery, which could have important clinical implications. PMID:26684070

  12. Gallic acid improved behavior, brain electrophysiology, and inflammation in a rat model of traumatic brain injury.

    PubMed

    Sarkaki, Alireza; Farbood, Yaghoub; Gharib-Naseri, Mohammad Kazem; Badavi, Mohammad; Mansouri, Mohammad Taghi; Haghparast, Abbas; Mirshekar, Mohammad Ali

    2015-08-01

    Traumatic brain injury (TBI) is one of the main causes of intellectual and cognitive disabilities. In the clinic it is essential to limit the development of cognitive impairment after TBI. In this study, the effects of gallic acid (GA; 100 mg/kg, per oral, from 7 days before to 2 days after TBI induction) on neurological score, passive avoidance memory, long-term potentiation (LTP) deficits, and levels of proinflammatory cytokines including interleukin-1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α) in the brain have been evaluated. Brain injury was induced following Marmarou's method. Data were analyzed by one-way and repeated measures ANOVA followed by Tukey's post-hoc test. The results indicated that memory was significantly impaired (p < 0.001) in the group treated with TBI + vehicle, together with deterioration of the hippocampal LTP and increased brain tissue levels of IL-1β, IL-6, and TNF-α. GA treatment significantly improved memory and LTP in the TBI rats. The brain tissue levels of IL-1β, IL-6, and TNF-α were significantly reduced (p < 0.001) in the group treated with GA. The results suggest that GA has neuroprotective properties against TBI-induced behavioral, electrophysiological, and inflammatory disorders, probably via the decrease of cerebral proinflammatory cytokines.

  13. Cerebral Edema in Traumatic Brain Injury: Pathophysiology and Prospective Therapeutic Targets.

    PubMed

    Winkler, Ethan A; Minter, Daniel; Yue, John K; Manley, Geoffrey T

    2016-10-01

    Traumatic brain injury is a heterogeneous disorder resulting from an external force applied to the head. The development of cerebral edema plays a central role in the evolution of injury following brain trauma and is closely associated with neurologic outcomes. Recent advances in the understanding of the molecular and cellular pathways contributing to the posttraumatic development of cerebral edema have led to the identification of multiple prospective therapeutic targets. The authors summarize the pathogenic mechanisms underlying cerebral edema and highlight the molecular pathways that may be therapeutically targeted to mitigate cerebral edema and associated sequelae following traumatic brain injury. PMID:27637397

  14. Investigating Metacognition, Cognition, and Behavioral Deficits of College Students with Acute Traumatic Brain Injuries

    ERIC Educational Resources Information Center

    Martinez, Sarah; Davalos, Deana

    2016-01-01

    Objective: Executive dysfunction in college students who have had an acute traumatic brain injury (TBI) was investigated. The cognitive, behavioral, and metacognitive effects on college students who endorsed experiencing a brain injury were specifically explored. Participants: Participants were 121 college students who endorsed a mild TBI, and 121…

  15. Structural Dissociation of Attentional Control and Memory in Adults with and without Mild Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Niogi, Sumit N.; Mukherjee, Pratik; Ghajar, Jamshid; Johnson, Carl E.; Kolster, Rachel; Lee, Hana; Suh, Minah; Zimmerman, Robert D.; Manley, Geoffrey T.; McCandliss, Bruce D.

    2008-01-01

    Memory and attentional control impairments are the two most common forms of dysfunction following mild traumatic brain injury (TBI) and lead to significant morbidity in patients, yet these functions are thought to be supported by different brain networks. This 3 T magnetic resonance diffusion tensor imaging (DTI) study investigates whether…

  16. Neuroimaging in Pediatric Traumatic Brain Injury: Current and Future Predictors of Functional Outcome

    ERIC Educational Resources Information Center

    Suskauer, Stacy J.; Huisman, Thierry A. G. M.

    2009-01-01

    Although neuroimaging has long played a role in the acute management of pediatric traumatic brain injury (TBI), until recently, its use as a tool for understanding and predicting long-term brain-behavior relationships after TBI has been limited by the relatively poor sensitivity of routine clinical imaging for detecting diffuse axonal injury…

  17. Getting My Bearings, Returning to School: Issues Facing Adolescents with Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Schilling, Ethan J.; Getch, Yvette Q.

    2012-01-01

    Traumatic brain injury (TBI) is characterized by a blow to the head or other penetrating head injury resulting in impairment of the brain's functioning. Despite the high incidence of TBI in adolescents, many educators still consider TBI to be a low-incidence disability. In addition, school personnel often report receiving little to no pre-service…

  18. Resting state magnetoencephalography functional connectivity in traumatic brain injury

    PubMed Central

    Tarapore, Phiroz E.; Findlay, Anne M.; LaHue, Sara C.; Lee, Hana; Honma, Susanne M.; Mizuiri, Danielle; Luks, Tracy L.; Manley, Geoffrey T.; Nagarajan, Srikantan S.; Mukherjee, Pratik

    2014-01-01

    Object Traumatic brain injury (TBI) is one of the leading causes of morbidity worldwide. One mechanism by which blunt head trauma may disrupt normal cognition and behavior is through alteration of functional connectivity between brain regions. In this pilot study, the authors applied a rapid automated resting state magnetoencephalography (MEG) imaging technique suitable for routine clinical use to test the hypothesis that there is decreased functional connectivity in patients with TBI compared with matched controls, even in cases of mild TBI. Furthermore, they posit that these abnormal reductions in MEG functional connectivity can be detected even in TBI patients without specific evidence of traumatic lesions on 3-T MR images. Finally, they hypothesize that the reductions of functional connectivity can improve over time across serial MEG scans during recovery from TBI. Methods Magnetoencephalography maps of functional connectivity in the alpha (8- to 12-Hz) band from 21 patients who sustained a TBI were compared with those from 18 age- and sex-matched controls. Regions of altered functional connectivity in each patient were detected in automated fashion through atlas-based registration to the control database. The extent of reduced functional connectivity in the patient group was tested for correlations with clinical characteristics of the injury as well as with findings on 3-T MRI. Finally, the authors compared initial connectivity maps with 2-year follow-up functional connectivity in a subgroup of 5 patients with TBI. Results Fourteen male and 7 female patients (17–53 years old, median 29 years) were enrolled. By Glasgow Coma Scale (GCS) criteria, 11 patients had mild, 1 had moderate, and 3 had severe TBI, and 6 had no GCS score recorded. On 3-T MRI, 16 patients had abnormal findings attributable to the trauma and 5 had findings in the normal range. As a group, the patients with TBI had significantly lower functional connectivity than controls (p < 0.01). Three

  19. Multicolor Fluorescence Imaging of Traumatic Brain Injury in a Cryolesion Mouse Model

    PubMed Central

    2012-01-01

    Traumatic brain injury is characterized by initial tissue damage, which then can lead to secondary processes such as cell death and blood-brain-barrier disruption. Clinical and preclinical studies of traumatic brain injury typically employ anatomical imaging techniques and there is a need for new molecular imaging methods that provide complementary biochemical information. Here, we assess the ability of a targeted, near-infrared fluorescent probe, named PSS-794, to detect cell death in a brain cryolesion mouse model that replicates certain features of traumatic brain injury. In short, the model involves brief contact of a cold rod to the head of a living, anesthetized mouse. Using noninvasive whole-body fluorescence imaging, PSS-794 permitted visualization of the cryolesion in the living animal. Ex vivo imaging and histological analysis confirmed PSS-794 localization to site of brain cell death. The nontargeted, deep-red Tracer-653 was validated as a tracer dye for monitoring blood-brain-barrier disruption, and a binary mixture of PSS-794 and Tracer-653 was employed for multicolor imaging of cell death and blood-brain-barrier permeability in a single animal. The imaging data indicates that at 3 days after brain cryoinjury the amount of cell death had decreased significantly, but the integrity of the blood-brain-barrier was still impaired; at 7 days, the blood-brain-barrier was still three times more permeable than before cryoinjury. PMID:22860222

  20. Traumatic brain injury: a disease process, not an event.

    PubMed

    Masel, Brent E; DeWitt, Douglas S

    2010-08-01

    Traumatic brain injury (TBI) is seen by the insurance industry and many health care providers as an "event." Once treated and provided with a brief period of rehabilitation, the perception exists that patients with a TBI require little further treatment and face no lasting effects on the central nervous system or other organ systems. In fact, TBI is a chronic disease process, one that fits the World Health Organization definition as having one or more of the following characteristics: it is permanent, caused by non-reversible pathological alterations, requires special training of the patient for rehabilitation, and/or may require a long period of observation, supervision, or care. TBI increases long-term mortality and reduces life expectancy. It is associated with increased incidences of seizures, sleep disorders, neurodegenerative diseases, neuroendocrine dysregulation, and psychiatric diseases, as well as non-neurological disorders such as sexual dysfunction, bladder and bowel incontinence, and systemic metabolic dysregulation that may arise and/or persist for months to years post-injury. The purpose of this article is to encourage the classification of TBI as the beginning of an ongoing, perhaps lifelong process, that impacts multiple organ systems and may be disease causative and accelerative. Our intent is not to discourage patients with TBI or their families and caregivers, but rather to emphasize that TBI should be managed as a chronic disease and defined as such by health care and insurance providers. Furthermore, if the chronic nature of TBI is recognized by government and private funding agencies, research can be directed at discovering therapies that may interrupt the disease processes months or even years after the initiating event. PMID:20504161

  1. Fatal traumatic brain injury, West Virginia, 1989-1998.

    PubMed Central

    Adekoya, Nelson; Majumder, Ranjit

    2004-01-01

    OBJECTIVE: The objective of this study was to describe fatal cases of traumatic brain injury (TBI) among West Virginia residents. METHODS: The authors analyzed data from the National Center for Health Statistics Multiple Cause of Death tapes for the period 1989-1998. They compared West Virginia's annualized average TBI death rate with the rates of other states and with the rate among U.S. residents for the same period. U.S. Bureau of Census population estimates were used as denominators. RESULTS: A total of 4,416 TBI deaths occurred in West Virginia in 1989-1998, for an annual average death rate of 23.6 per 100,000 population. From 1989 to 1998, TBI death rates declined 5% (p=0.4042). Seventy-five percent (n=3,315) of fatalities occurred among men. Adults > or =65 years of age accounted for the highest percentage of fatal injuries (n=1,135). The leading external causes of fatal TBI were: firearm-related (39% of reported fatalities), motor vehicles-related (34%), and fall-related (10%). Firearm-related TBI became the leading cause of TBI fatalities in 1991, surpassing motor vehicle-related TBI. Seventy-five percent of firearm-related TBI deaths were suicides (n=1,302). West Virginia's TBI death rate (23.6 per 100,000) was higher than the national rate (20.6 per 100,000). In 23 states, the average TBI death rates over the 10-year period were higher than West Virginia's. Whereas modest declines in TBI death rates occurred for motor vehicle-related and firearm-related causes in West Virginia, a concomitant 38% increase occurred in the fall-related TBI death rate during the decade. CONCLUSION: Data presented in this report can be used to develop targeted prevention programs in West Virginia. PMID:15313112

  2. ED Utilization Trends in Sports-Related Traumatic Brain Injury

    PubMed Central

    Pomerantz, Wendy J.; Gittelman, Mike

    2013-01-01

    BACKGROUND: Emergency department (ED) visits for sports-related traumatic brain injuries (TBIs) have risen. This study evaluated how the number and severity of admissions have changed as ED visits for sports-related TBIs have increased. METHODS: A retrospective study of children aged 0 to 19 years at a level 1 trauma center was performed. Patients from 2002 to 2011 with a primary or secondary diagnosis of TBI were identified from the hospital’s inpatient and outpatient trauma registries. Frequencies were used to characterize the population, χ2 analysis was performed to determine differences between groups, and regression analysis looked at relationship between year and injury severity score or length of stay. RESULTS: Sport was responsible for injury in 3878 (15.4%) cases during the study period; 3506 (90.4%) were discharged from the hospital, and 372 (9.6%) were admitted. Seventy-three percent were male patients and 78% Caucasian; mean age was 13 ± 3.5 years. ED visits for sports-related TBIs increased 92% over the study period, yet there was no significant change (χ2 = 9.8, df = 9, P = .37) in the percentage of children admitted. Mean injury severity score for those admitted decreased from 7.8 to 4.8 (β = –0.46; P = .006); length of stay trended downward (β = –0.05; P = .05). CONCLUSIONS: The percentage of children being admitted from the ED with sports-related TBI has not changed over the past 10 years. The severity of admitted sports-related TBI is decreasing. Additional research is needed to correlate these trends with other TBI mechanisms. PMID:24081999

  3. Rodent Models of Traumatic Brain Injury: Methods and Challenges.

    PubMed

    Marklund, Niklas

    2016-01-01

    Traumatic brain injury (TBI) has been named the most complex disease in the most complex organ of the body. It is the most common cause of death and disability in the Western world in people <40 years old and survivors commonly suffer from persisting cognitive deficits, impaired motor function, depression and personality changes. TBI may vary in severity from uniformly fatal to mild injuries with rapidly resolving symptoms and without doubt, it is a markedly heterogeneous disease. Its different subtypes differs in their pathophysiology, treatment options and long-term consequences and to date, there are no pharmacological treatments with proven clinical benefit available to TBI patients. To enable development of novel treatment options for TBI, clinically relevant animal models are needed. Due to their availability and low costs, numerous rodent models have been developed which have substantially contributed to our current understanding of the pathophysiology of TBI. The most common animal models used in laboratories worldwide are likely the controlled cortical impact (CCI) model, the central and lateral fluid percussion injury (FPI) models, and weight drop/impact acceleration (I/A) models. Each of these models has inherent advantages and disadvantages; these need to be thoroughly considered when selecting the rodent TBI model according to the hypothesis and design of the study. Since TBI is not one disease, refined animal models must take into account the clinical features and complexity of human TBI. To enhance the possibility of establishing preclinical efficacy of a novel treatment, the preclinical use of several different experimental models is encouraged as well as varying the species, gender, and age of the animal. In this chapter, the methods, limitations, and challenges of the CCI and FPI models of TBI used in rodents are described. PMID:27604711

  4. Persistent Pain in Adolescents Following Traumatic Brain Injury

    PubMed Central

    Tham, See Wan; Palermo, Tonya M.; Wang, Jin; Jaffe, Kenneth M.; Temkin, Nancy; Durbin, Dennis; Rivara, Frederick P.

    2014-01-01

    Traumatic brain injury (TBI) is a leading cause of pediatric disability. Although persistent pain has been recognized as a significant postinjury complication, there is a paucity of data concerning the postinjury pain experience of youth. This study aimed to examine the prevalence of persistent pain in adolescents after TBI, identify risk factors for pain, and evaluate the impact of pain on adolescent health-related quality of life. Participants included 144 adolescents with mild to severe TBI who were followed over 36 months after injury. At 3-, 12-, 24-, and 36-month assessments, measures of pain intensity, depression, posttraumatic stress disorder, and health-related quality of life were completed by adolescents. Findings demonstrated that 24.3% of adolescents reported persistent pain (defined as usual pain intensity ≥3/10) at all assessment points after TBI. Female sex (odds ratio = 2.73, 95% confidence interval = 1.12–6.63) and higher levels of depressive symptoms at 3 months after injury (odds ratio = 1.26, 95% confidence interval = 1.12–1.43) were predictors of persistent pain at 36 months. Furthermore, mixed linear models indicated that early pain experience at 3 months following TBI was associated with a significantly poorer long-term health-related quality of life. Perspective This is the first study to examine the prevalence of persistent pain over long-term follow-up in adolescents after TBI and its impact on health-related quality of life. These findings indicate that adolescents with TBI may benefit from timely evaluation and intervention to minimize the development and impact of pain. PMID:23911979

  5. GH and Pituitary Hormone Alterations After Traumatic Brain Injury.

    PubMed

    Karaca, Züleyha; Tanrıverdi, Fatih; Ünlühızarcı, Kürşad; Kelestimur, Fahrettin

    2016-01-01

    Traumatic brain injury (TBI) is a crucially important public health problem around the world, which gives rise to increased mortality and is the leading cause of physical and psychological disability in young adults, in particular. Pituitary dysfunction due to TBI was first described 95 years ago. However, until recently, only a few papers have been published in the literature and for this reason, TBI-induced hypopituitarism has been neglected for a long time. Recent studies have revealed that TBI is one of the leading causes of hypopituitarism. TBI which causes hypopituitarism may be characterized by a single head injury such as from a traffic accident or by chronic repetitive head trauma as seen in combative sports including boxing, kickboxing, and football. Vascular damage, hypoxic insult, direct trauma, genetic predisposition, autoimmunity, and neuroinflammatory changes may have a role in the development of hypopituitarism after TBI. Because of the exceptional structure of the hypothalamo-pituitary vasculature and the special anatomic location of anterior pituitary cells, GH is the most commonly lost hormone after TBI, and the frequency of isolated GHD is considerably high. TBI-induced pituitary dysfunction remains undiagnosed and therefore untreated in most patients because of the nonspecific and subtle clinical manifestations of hypopituitarism. Treatment of TBI-induced hypopituitarism depends on the deficient anterior pituitary hormones. GH replacement therapy has some beneficial effects on metabolic parameters and neurocognitive dysfunction. Patients with TBI without neuroendocrine changes and those with TBI-induced hypopituitarism share the same clinical manifestations, such as attention deficits, impulsion impairment, depression, sleep abnormalities, and cognitive disorders. For this reason, TBI-induced hypopituitarism may be neglected in TBI victims and it would be expected that underlying hypopituitarism would aggravate the clinical picture of TBI

  6. Naloxone for Severe Traumatic Brain Injury: A Meta-Analysis

    PubMed Central

    Du, Renfei; Xu, Enxi; Dong, Lun; Wang, Xingdong; Yan, Zhengcun; Pang, Lujun; Wei, Min; She, Lei

    2014-01-01

    Objective The efficiency of naloxone for the management of secondary brain injury after severe traumatic brain injury (sTBI) remains undefined. The aim of this study is to evaluate the current evidence regarding the clinical efficiency and safety of naloxone as a treatment for sTBI in mainland China. Methodology/Principal Findings A systematic search of the China Biology Medicine disc (CBM), China Science and Technology Journal Database (VIP), China National Knowledge Internet (CNKI), and Wan Fang Database was performed to identify randomized controlled trials (RCTs) of naloxone treatment for patients with sTBI in mainland China. The quality of the included trials was assessed, and the RevMan 5.1 software was employed to conduct this meta-analysis. Nineteen RCTs including 2332 patients were included in this study. The odds ratio (OR) showed statistically significant differences between the naloxone group and the control group (placebo) in terms of mortality at 18 months after treatment (OR, 0.51, 95%CI: 0.38–0.67; p<0.00001), prevalence of abnormal heart rates (OR, 0.30, 95%CI: 0.21–0.43; p<0.00001), abnormal breathing rate (OR, 0.25, 95%CI: 0.17–0.36; p<0.00001) at discharge, the level of intracranial pressure at discharge (OR, 2.00, 95%CI: 1.41–2.83; p = 0.0001), verbal or physical dysfunction rate (OR, 0.65, 95%CI: 0.43–0.98; p = 0.04), and severe disability rate (OR, 0.47, 95%CI: 0.30–0.73; p = 0.0001) at 18 months after the treatment. The mean difference (MD) showed statistically significant differences in awakening time at discharge (MD, −4.81, 95%CI: −5.49 to −4.12; p<0.00001), and GCS at 3 days (MD, 1.00, 95%CI: 0.70–1.30; p<0.00001) and 10 days (MD, 1.76, 95%CI: 1.55–1.97; p<0.00001) after treatment comparing naloxone with placebo group. Conclusions/Significance This study indicated that applying naloxone in the early stage for sTBI patients might effectively reduce mortality, control intracranial pressure (ICP), and

  7. Motorcycle-Related Traumatic Brain Injuries: Helmet Use and Treatment Outcome

    PubMed Central

    Nnadi, Mathias Ogbonna Nnanna; Bankole, Olufemi Babatola; Fente, Beleudanyo Gbalipre

    2015-01-01

    Summary. With increasing use of motorcycle as means of transport in developing countries, traumatic brain injuries from motorcycle crashes have been increasing. The only single gadget that protects riders from traumatic brain injury is crash helmet. Objective. The objectives were to determine the treatment outcome among traumatic brain injury patients from motorcycle crashes and the rate of helmet use among them. Methods. It was a prospective, cross-sectional study of motorcycle-related traumatic brain injury patients managed in our center from 2010 to 2014. Patients were managed using our unit protocol for traumatic brain injuries. Data for the study were collected in accident and emergency, intensive care unit, wards, and outpatient clinic. The data were analyzed using Environmental Performance Index (EPI) info 7 software. Results. Ninety-six patients were studied. There were 87 males. Drivers were 65. Only one patient wore helmet. Majority of them were between 20 and 40 years. Fifty-three patients had mild head injuries. Favorable outcome among them was 84.35% while mortality was 12.5%. Severity of the injury affected the outcome significantly. Conclusion. Our study showed that the helmet use by motorcycle riders was close to zero despite the existing laws making its use compulsory in Nigeria. The outcome was related to severity of injuries. PMID:26317112

  8. Influence of Post-Traumatic Stress Disorder on Neuroinflammation and Cell Proliferation in a Rat Model of Traumatic Brain Injury

    PubMed Central

    Diamond, David M.; Shinozuka, Kazutaka; Ishikawa, Hiroto; Hernandez, Diana G.; Sanberg, Paul R.; Kaneko, Yuji; Borlongan, Cesar V.

    2013-01-01

    Long-term consequences of traumatic brain injury (TBI) are closely associated with the development of severe psychiatric disorders, such as post-traumatic stress disorder (PTSD), yet preclinical studies on pathological changes after combined TBI with PTSD are lacking. In the present in vivo study, we assessed chronic neuroinflammation, neuronal cell loss, cell proliferation and neuronal differentiation in specific brain regions of adult Sprague-Dawley male rats following controlled cortical impact model of moderate TBI with or without exposure to PTSD. Eight weeks post-TBI, stereology-based histological analyses revealed no significant differences between sham and PTSD alone treatment across all brain regions examined, whereas significant exacerbation of OX6-positive activated microglial cells in the striatum, thalamus, and cerebral peduncle, but not cerebellum, in animals that received TBI alone and combined TBI-PTSD compared with PTSD alone and sham treatment. Additional immunohistochemical results revealed a significant loss of CA3 pyramidal neurons in the hippocampus of TBI alone and TBI-PTSD compared to PTSD alone and sham treatment. Further examination of neurogenic niches revealed a significant downregulation of Ki67-positive proliferating cells, but not DCX-positive neuronally migrating cells in the neurogenic subgranular zone and subventricular zone for both TBI alone and TBI-PTSD compared to PTSD alone and sham treatment. Comparisons of levels of neuroinflammation and neurogenesis between TBI alone and TBI+PTSD revealed that PTSD did not exacerbate the neuropathological hallmarks of TBI. These results indicate a progressive deterioration of the TBI brain, which, under the conditions of the present approach, was not intensified by PTSD, at least within our time window and within the examined areas of the brain. Although the PTSD manipulation employed here did not exacerbate the pathological effects of TBI, the observed long-term inflammation and suppressed

  9. Mismatch negativity, social cognition, and functional outcomes in patients after traumatic brain injury

    PubMed Central

    Sun, Hui-yan; Li, Qiang; Chen, Xi-ping; Tao, Lu-yang

    2015-01-01

    Mismatch negativity is generated automatically, and is an early monitoring indicator of neuronal integrity impairment and functional abnormality in patients with brain injury, leading to decline of cognitive function. Antipsychotic medication cannot affect mismatch negativity. The present study aimed to explore the relationships of mismatch negativity with neurocognition, daily life and social functional outcomes in patients after brain injury. Twelve patients with traumatic brain injury and 12 healthy controls were recruited in this study. We examined neurocognition with the Wechsler Adult Intelligence Scale-Revised China, and daily and social functional outcomes with the Activity of Daily Living Scale and Social Disability Screening Schedule, respectively. Mismatch negativity was analyzed from electroencephalogram recording. The results showed that mismatch negativity amplitudes decreased in patients with traumatic brain injury compared with healthy controls. Mismatch negativity amplitude was negatively correlated with measurements of neurocognition and positively correlated with functional outcomes in patients after traumatic brain injury. Further, the most significant positive correlations were found between mismatch negativity in the fronto-central region and measures of functional outcomes. The most significant positive correlations were also found between mismatch negativity at the FCz electrode and daily living function. Mismatch negativity amplitudes were extremely positively associated with Social Disability Screening Schedule scores at the Fz electrode in brain injury patients. These experimental findings suggest that mismatch negativity might efficiently reflect functional outcomes in patients after traumatic brain injury. PMID:26170824

  10. Mismatch negativity, social cognition, and functional outcomes in patients after traumatic brain injury.

    PubMed

    Sun, Hui-Yan; Li, Qiang; Chen, Xi-Ping; Tao, Lu-Yang

    2015-04-01

    Mismatch negativity is generated automatically, and is an early monitoring indicator of neuronal integrity impairment and functional abnormality in patients with brain injury, leading to decline of cognitive function. Antipsychotic medication cannot affect mismatch negativity. The present study aimed to explore the relationships of mismatch negativity with neurocognition, daily life and social functional outcomes in patients after brain injury. Twelve patients with traumatic brain injury and 12 healthy controls were recruited in this study. We examined neurocognition with the Wechsler Adult Intelligence Scale-Revised China, and daily and social functional outcomes with the Activity of Daily Living Scale and Social Disability Screening Schedule, respectively. Mismatch negativity was analyzed from electroencephalogram recording. The results showed that mismatch negativity amplitudes decreased in patients with traumatic brain injury compared with healthy controls. Mismatch negativity amplitude was negatively correlated with measurements of neurocognition and positively correlated with functional outcomes in patients after traumatic brain injury. Further, the most significant positive correlations were found between mismatch negativity in the fronto-central region and measures of functional outcomes. The most significant positive correlations were also found between mismatch negativity at the FCz electrode and daily living function. Mismatch negativity amplitudes were extremely positively associated with Social Disability Screening Schedule scores at the Fz electrode in brain injury patients. These experimental findings suggest that mismatch negativity might efficiently reflect functional outcomes in patients after traumatic brain injury. PMID:26170824

  11. Diffusion Tensor Imaging of Incentive Effects in Prospective Memory after Pediatric Traumatic Brain Injury

    PubMed Central

    Wilde, Elisabeth A.; Bigler, Erin D.; Chu, Zili; Yallampalli, Ragini; Oni, Margaret B.; Wu, Trevor C.; Ramos, Marco A.; Pedroza, Claudia; Vásquez, Ana C.; Hunter, Jill V.; Levin, Harvey S.

    2011-01-01

    Abstract Few studies exist investigating the brain-behavior relations of event-based prospective memory (EB-PM) impairments following traumatic brain injury (TBI). To address this, children with moderate-to-severe TBI performed an EB-PM test with two motivational enhancement conditions and underwent concurrent diffusion tensor imaging (DTI) at 3 months post-injury. Children with orthopedic injuries (OI; n = 37) or moderate-to-severe TBI (n = 40) were contrasted. Significant group differences were found for fractional anisotropy (FA) and apparent diffusion coefficient for orbitofrontal white matter (WM), cingulum bundles, and uncinate fasciculi. The FA of these WM structures in children with TBI significantly correlated with EB-PM performance in the high, but not the low motivation condition. Regression analyses within the TBI group indicated that the FA of the left cingulum bundle (p = 0.003), left orbitofrontal WM (p < 0.02), and left (p < 0.02) and right (p < 0.008) uncinate fasciculi significantly predicted EB-PM performance in the high motivation condition. We infer that the cingulum bundles, orbitofrontal WM, and uncinate fasciculi are important WM structures mediating motivation-based EB-PM responses following moderate-to-severe TBI in children. PMID:21250917

  12. Abnormal White Matter Blood-Oxygen-Level–Dependent Signals in Chronic Mild Traumatic Brain Injury

    PubMed Central

    Astafiev, Serguei V.; Shulman, Gordon L.; Metcalf, Nicholas V.; Rengachary, Jennifer; MacDonald, Christine L.; Harrington, Deborah L.; Maruta, Jun; Shimony, Joshua S.; Ghajar, Jamshid; Diwakar, Mithun; Huang, Ming-Xiong; Lee, Roland R.

    2015-01-01

    Abstract Concussion, or mild traumatic brain injury (mTBI), can cause persistent behavioral symptoms and cognitive impairment, but it is unclear if this condition is associated with detectable structural or functional brain changes. At two sites, chronic mTBI human subjects with persistent post-concussive symptoms (three months to five years after injury) and age- and education-matched healthy human control subjects underwent extensive neuropsychological and visual tracking eye movement tests. At one site, patients and controls also performed the visual tracking tasks while blood-oxygen-level–dependent (BOLD) signals were measured with functional magnetic resonance imaging. Although neither neuropsychological nor visual tracking measures distinguished patients from controls at the level of individual subjects, abnormal BOLD signals were reliably detected in patients. The most consistent changes were localized in white matter regions: anterior internal capsule and superior longitudinal fasciculus. In contrast, BOLD signals were normal in cortical regions, such as the frontal eye field and intraparietal sulcus, that mediate oculomotor and attention functions necessary for visual tracking. The abnormal BOLD signals accurately differentiated chronic mTBI patients from healthy controls at the single-subject level, although they did not correlate with symptoms or neuropsychological performance. We conclude that subjects with persistent post-concussive symptoms can be identified years after their TBI using fMRI and an eye movement task despite showing normal structural MRI and DTI. PMID:25758167

  13. Free-Radical Scavenger Edaravone Treatment Confers Neuroprotection Against Traumatic Brain Injury in Rats

    PubMed Central

    Wang, Guo-Hua; Li, Yong-Cai; Li, Xia; Shi, Hong; Gao, Yan-Qin; Vosler, Peter S.

    2011-01-01

    Abstract Traumatic brain injury (TBI) is one of the leading causes of neurological disability in young adults. Edaravone, a novel synthetic small-molecule free-radical scavenger, has been shown to have a neuroprotective effect in both animal models of cerebral ischemia and stroke patients; however, the underlying mechanism is poorly understood. In this report, we investigated the potential mechanisms of edaravone treatment in a rat model of TBI. TBI was induced in the right cerebral cortex of male adult rats using Feeney's weight-drop method. Edaravone (0.75, 1.5, or 3 mg/kg) or vehicle (normal saline) was intravenously administered at 2 and 12 h after TBI. Edaravone treatment significantly decreased hippocampal CA3 neuron loss, reduced oxidative stress, and decreased neuronal programmed cell death compared to vehicle treatment. The protective effects of edaravone treatment were also related to the pathology of TBI on non-neuronal cells, as edaravone decreased astrocyte and glial activation. Lastly, edaravone treatment significantly reduced the presence of inflammatory cytokines, cerebral edema, blood–brain barrier (BBB) permeability, and, importantly, neurological deficits following TBI. Our results suggest that edaravone exerts a neuroprotective effect in the rat model of TBI. The likely mechanism is via inhibiting oxidative stress, leading to a decreased inflammatory response and glial activation, and thereby reducing neuronal death and improving neurological function. PMID:21732763

  14. Common Data Elements for Pediatric Traumatic Brain Injury: Recommendations from the Biospecimens and Biomarkers Workgroup

    PubMed Central

    Beers, Sue R.; Papa, Linda; Bell, Michael

    2012-01-01

    Abstract Biospecimens represent a critically important resource in pediatric brain injury research. Data from these specimens can be used to identify and classify injury, understand the molecular mechanisms underlying different types of brain injury, and ultimately identify therapeutic targets to tailor treatments for individual patient needs. To realize the full potential of biospecimens in pediatric traumatic brain injury (TBI), standardization and adoption of best practice guidelines are needed to ensure the quality and consistency of specimens. Multiple groups, including the National Cancer Institute (NCI), the International Society for Biological and Environmental Repositories (ISBER), and the Organisation for Economic Co-operation and Development (OECD), have previously published best practice guidelines for biospecimen resources. Recommendations have also been provided by the Biospecimens and Biomarkers Workgroup of the interagency TBI Common Data Elements (CDE) initiative. The recommendations from all of these sources, however, focus exclusively on adult biospecimen collection. There are no published pediatric-specific biospecimen collection guidelines. An additional workgroup was formed to specifically address this gap. The aim of the Pediatric TBI CDE Biospecimens and Biomarkers Workgroup was to provide recommendations for best practice guidelines to standardize the quality and accessibility of biospecimens for pediatric brain injury research in general, and for pediatric TBI research in particular. Consensus recommendations were developed by review of previously published adult-specific recommendations, including the recommendations of the original TBI Common Data Elements Biospecimens and Biomarkers Workgroup, and by participation in the interagency workshop “Common Data Elements for TBI Research: Pediatric Considerations,” held in Houston, Texas in March of 2010. These recommendations represent expert opinion on this subject. The authors of this

  15. Neuronal DNA Methylation Profiling of Blast-Related Traumatic Brain Injury

    PubMed Central

    Ge, Yongchao; Chen, Sean; Xin, Yurong; Umali, Michelle U.; De Gasperi, Rita; Gama Sosa, Miguel A.; Ahlers, Stephen T.; Elder, Gregory A.

    2015-01-01

    Abstract Long-term molecular changes in the brain resulting from blast exposure may be mediated by epigenetic changes, such as deoxyribonucleic acid (DNA) methylation, that regulate gene expression. Aberrant regulation of gene expression is associated with behavioral abnormalities, where DNA methylation bridges environmental signals to sustained changes in gene expression. We assessed DNA methylation changes in the brains of rats exposed to three 74.5 kPa blast overpressure events, conditions that have been associated with long-term anxiogenic manifestations weeks or months following the initial exposures. Rat frontal cortex eight months post-exposure was used for cell sorting of whole brain tissue into neurons and glia. We interrogated DNA methylation profiles in these cells using Expanded Reduced Representation Bisulfite Sequencing. We obtained data for millions of cytosines, showing distinct methylation profiles for neurons and glia and an increase in global methylation in neuronal versus glial cells (p<10−7). We detected DNA methylation perturbations in blast overpressure–exposed animals, compared with sham blast controls, within 458 and 379 genes in neurons and glia, respectively. Differentially methylated neuronal genes showed enrichment in cell death and survival and nervous system development and function, including genes involved in transforming growth factor β and nitric oxide signaling. Functional validation via gene expression analysis of 30 differentially methylated neuronal and glial genes showed a 1.2 fold change in gene expression of the serotonin N-acetyltransferase gene (Aanat) in blast animals (p<0.05). These data provide the first genome-based evidence for changes in DNA methylation induced in response to multiple blast overpressure exposures. In particular, increased methylation and decreased gene expression were observed in the Aanat gene, which is involved in converting serotonin to the circadian hormone melatonin and is implicated in

  16. Paradoxical facilitation of a free recall of nonwords in persons with traumatic brain injury.

    PubMed

    Toomela, A; Tomberg, T; Orasson, A; Tikk, A; Nõmm, M

    1999-04-01

    Brain damage is usually associated with behavioral deficits. However, there is an increasing amount of evidence that lesions of some brain regions are associated with improvements instead of impairments of certain behaviors. We report the results of a study of free recall performance in subjects with traumatic brain injury. One-fourth of the subjects displayed above-normal performance in recall of nonwords. No such facilitation was found with nine lists of words. PMID:10101040

  17. Therapeutic Hypothermia as a Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Brain Injury and Traumatic Brain Injury

    PubMed Central

    Ma, H.; Sinha, B.; Pandya, R.S.; Lin, N.; Popp, A.J.; Li, J.; Yao, J.; Wang, X.

    2014-01-01

    Evidence shows that artificially lowering body and brain temperature can significantly reduce the deleterious effects of brain injury in both newborns and adults. Although the benefits of therapeutic hypothermia have long been known and applied clinically, the underlying molecular mechanisms have yet to be elucidated. Hypoxic-ischemic brain injury and traumatic brain injury both trigger a series of biochemical and molecular events that cause additional brain insult. Induction of therapeutic hypothermia seems to ameliorate the molecular cascade that culminates in neuronal damage. Hypothermia attenuates the toxicity produced by the initial injury that would normally produce reactive oxygen species, neurotransmitters, inflammatory mediators, and apoptosis. Experiments have been performed on various depths and levels of hypothermia to explore neuroprotection. This review summarizes what is currently known about the beneficial effects of therapeutic hypothermia in experimental models of neonatal hypoxic-ischemic brain injury and traumatic brain injury, and explores the molecular mechanisms that could become the targets of novel therapies. In addition, this review summarizes the clinical implications of therapeutic hypothermia in newborn hypoxic-ischemic encephalopathy and adult traumatic brain injury. PMID:22834830

  18. Blast traumatic brain injury in the rat using a blast overpressure model.

    PubMed

    Yarnell, Angela M; Shaughness, Michael C; Barry, Erin S; Ahlers, Stephen T; McCarron, Richard M; Grunberg, Neil E

    2013-01-01

    Traumatic brain injury (TBI) is a serious health concern for civilians and military populations, and blast-induced TBI (bTBI) has become an increasing problem for military personnel over the past 10 years. To understand the biological and psychological effects of blast-induced injuries and to examine potential interventions that may help to prevent, attenuate, and treat effects of bTBI, it is valuable to conduct controlled animal experiments. This unit discusses available paradigms to model traumatic brain injury in animals, with an emphasis on the relevance of these various models to study blast-induced traumatic brain injury (bTBI). This paper describes the detailed methods of a blast overpressure (BOP) paradigm that has been used to conduct experiments with rats to model blast exposure. This particular paradigm models the pressure wave created by explosions, including improvised explosive devices (IEDs).

  19. Water-soluble progesterone analogues are effective, injectable treatments in animal models of traumatic brain injury.

    PubMed

    Guthrie, David B; Stein, Donald G; Liotta, Dennis C; Lockwood, Mark A; Sayeed, Iqbal; Atif, Fahim; Arrendale, Richard F; Reddy, G Prabhakar; Evers, Taylor J; Marengo, Jose R; Howard, Randy B; Culver, Deborah G; Natchus, Michael G

    2012-05-10

    After more than 30 years of research and 30 failed clinical trials with as many different treatments, progesterone is the first agent to demonstrate robust clinical efficacy as a treatment for traumatic brain injuries. It is currently being investigated in two, independent phase III clinical trials in hospital settings; however, it presents a formidable solubility challenge that has so far prevented the identification of a formulation that would be suitable for emergency field response use or battlefield situations. Accordingly, we have designed and tested a novel series of water-soluble analogues that address this critical need. We report here the synthesis of C-20 oxime conjugates of progesterone as therapeutic agents for traumatic brain injuries with comparable efficacy in animal models of traumatic brain injury and improved solubility and pharmacokinetic profiles. Pharmacodynamic analysis reveals that a nonprogesterone steroidal analogue may be primarily responsible for the observed activity. PMID:24900479

  20. Medical-School Partnership in Guiding Return to School Following Mild Traumatic Brain Injury in Youth.

    PubMed

    Gioia, Gerard A

    2016-01-01

    Mild traumatic brain injury is recognized as a prevalent and significant risk concern for youth. Appropriate school return is particularly challenging. The medical and school systems must be prepared partners to support the school return of the student with mild traumatic brain injury. Medical providers must be trained in assessment and management skills with a focused understanding of school demands. Schools must develop policies and procedures to prepare staff to support a gradual return process with the necessary academic accommodations. Ongoing communication between the family, student, school, and medical provider is essential to supporting recovery. A systematic gradual return to school process is proposed including levels of recommended activity and criteria for advancement. Targets for intervention are described with associated strategies for supporting recovery. A 10-element Progressive Activities of Controlled Exertion (PACE) model for activity-exertion management is introduced to manage symptom exacerbation. A strong medical-school partnership will maximize outcomes for students with mild traumatic brain injury.

  1. Diminished supraspinal pain modulation in patients with mild traumatic brain injury

    PubMed Central

    Shukla, Shivshil; Yang, Eric; Canlas, Bryan; Kadokana, Mawj; Heald, Jason; Davani, Ariea; Song, David; Lin, Lisa; Polston, Greg; Tsai, Alice; Lee, Roland

    2016-01-01

    Background Chronic pain conditions are highly prevalent in patients with mild traumatic brain injury. Supraspinal diffuse axonal injury is known to dissociate brain functional connectivity in these patients. The effect of this dissociated state on supraspinal pain network is largely unknown. A functional magnetic resonance imaging study was conducted to compare the supraspinal pain network in patients with mild traumatic brain injury to the gender and age-matched healthy controls with the hypothesis that the functional connectivities of the medial prefrontal cortices, a supraspinal pain modulatory region to other pain-related sensory discriminatory and affective regions in the mild traumatic brain injury subjects are significantly reduced in comparison to healthy controls. Results The mild traumatic brain injury group (N = 15) demonstrated significantly (P < 0.01, cluster threshold > 150 voxels) less activities in the thalamus, pons, anterior cingulate cortex, insula, dorsolateral prefrontal cortex, and medial prefrontal cortices than the healthy control group (N = 15). Granger Causality Analyses (GCA) indicated while the left medial prefrontal cortices of the healthy control group cast a noticeable degree of outward (to affect) causality inference to multiple pain processing related regions, this outward inference pattern was not observed in the mild traumatic brain injury group. On the other hand, only patients’ bilateral anterior cingulate cortex received multiple inward (to be affected) causality inferences from regions including the primary and secondary somatosensory cortices and the inferior parietal lobe. Resting state functional connectivity analyses indicated that the medial prefrontal cortices of the mild traumatic brain injury group demonstrated a significantly (P < 0.01, F = 3.6, cluster size > 150 voxels) higher degree of functional connectivity to the inferior parietal lobe, premotor and secondary somatosensory cortex

  2. Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy.

    PubMed

    Puvenna, Vikram; Engeler, Madeline; Banjara, Manoj; Brennan, Chanda; Schreiber, Peter; Dadas, Aaron; Bahrami, Ashkon; Solanki, Jesal; Bandyopadhyay, Anasua; Morris, Jacqueline K; Bernick, Charles; Ghosh, Chaitali; Rapp, Edward; Bazarian, Jeffrey J; Janigro, Damir

    2016-01-01

    Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (P<0.01) but not between CTE and TLE (P=0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE. PMID:26556772

  3. Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy.

    PubMed

    Puvenna, Vikram; Engeler, Madeline; Banjara, Manoj; Brennan, Chanda; Schreiber, Peter; Dadas, Aaron; Bahrami, Ashkon; Solanki, Jesal; Bandyopadhyay, Anasua; Morris, Jacqueline K; Bernick, Charles; Ghosh, Chaitali; Rapp, Edward; Bazarian, Jeffrey J; Janigro, Damir

    2016-01-01

    Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (P<0.01) but not between CTE and TLE (P=0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE.

  4. [Differentiated treatment of isolated traumatic injury of frontal lobes of the brain].

    PubMed

    Smirnova, M M; Shcherbuk, Iu A; Morozov, S A

    2014-01-01

    An analysis of treatment results was made in 83 patients with traumatic parenchymatous injuries of frontal lobes of the brain. Surgical interventions were performed in 31 patients and the conservative therapy was carried out in 52 patients. Regular neurological examinations were completed for all the patients. The data of neurovisual methods were estimated. A strategy of treatment of frontal lobes injury depends on not only from the traumatic substratum volume, but at the same time, it is formed by clinical neurologic constellations and instrumental data in traumatic injury of frontal lobes of the brain. Risk factors of unfavorable effect of traumatic parenchymatous injury of frontal lobes of the brain were reflected in the initially low GCS score, a neurologic deficit progression with contusion haemorrhagic foci in the frontal lobe (volume greater than 25 cm3), a midline shift on 6 mm or more and signs of base cistern compression and presence of mass-effect, according to CT scan data. The developed algorithm could improve the results of treatment and makes better the quality of life of the patients with traumatic parenchymatous injuries of frontal lobes of the brain.

  5. Traumatic Brain Injury by a Closed Head Injury Device Induces Cerebral Blood Flow Changes and Microhemorrhages

    PubMed Central

    Kallakuri, Srinivasu; Bandaru, Sharath; Zakaria, Nisrine; Shen, Yimin; Kou, Zhifeng; Zhang, Liying; Haacke, Ewart Mark; Cavanaugh, John M

    2015-01-01

    Objectives: Traumatic brain injury is a poly-pathology characterized by changes in the cerebral blood flow, inflammation, diffuse axonal, cellular, and vascular injuries. However, studies related to understanding the temporal changes in the cerebral blood flow following traumatic brain injury extending to sub-acute periods are limited. In addition, knowledge related to microhemorrhages, such as their detection, localization, and temporal progression, is important in the evaluation of traumatic brain injury. Materials and Methods: Cerebral blood flow changes and microhemorrhages in male Sprague Dawley rats at 4 h, 24 h, 3 days, and 7 days were assessed following a closed head injury induced by the Marmarou impact acceleration device (2 m height, 450 g brass weight). Cerebral blood flow was measured by arterial spin labeling. Microhemorrhages were assessed by susceptibility-weighted imaging and Prussian blue histology. Results: Traumatic brain injury rats showed reduced regional and global cerebral blood flow at 4 h and 7 days post-injury. Injured rats showed hemorrhagic lesions in the cortex, corpus callosum, hippocampus, and brainstem in susceptibility-weighted imaging. Injured rats also showed Prussian blue reaction products in both the white and gray matter regions up to 7 days after the injury. These lesions were observed in various areas of the cortex, corpus callosum, hippocampus, thalamus, and midbrain. Conclusions: These results suggest that changes in cerebral blood flow and hemorrhagic lesions can persist for sub-acute periods after the initial traumatic insult in an animal model. In addition, microhemorrhages otherwise not seen by susceptibility-weighted imaging are present in diverse regions of the brain. The combination of altered cerebral blood flow and microhemorrhages can potentially be a source of secondary injury changes following traumatic brain injury and may need to be taken into consideration in the long-term care of these cases. PMID:26605126

  6. Acute neuroprotective effects of extremely low-frequency electromagnetic fields after traumatic brain injury in rats.

    PubMed

    Yang, Yang; Li, Ling; Wang, Yan-Gang; Fei, Zhou; Zhong, Jun; Wei, Li-Zhou; Long, Qian-Fa; Liu, Wei-Ping

    2012-05-10

    Traumatic brain injury commonly has a result of a short window of opportunity between the period of initial brain injury and secondary brain injury, which provides protective strategies and can reduce damages of brain due to secondary brain injury. Previous studies have reported neuroprotective effects of extremely low-frequency electromagnetic fields. However, the effects of extremely low-frequency electromagnetic fields on neural damage after traumatic brain injury have not been reported yet. The present study aims to investigate effects of extremely low-frequency electromagnetic fields on neuroprotection after traumatic brain injury. Male Sprague-Dawley rats were used for the model of lateral fluid percussion injury, which were placed in non-electromagnetic fields and 15 Hz (Hertz) electromagnetic fields with intensities of 1 G (Gauss), 3 G and 5 G. At various time points (ranging from 0.5 to 30 h) after lateral fluid percussion injury, rats were treated with kainic acid (administered by intraperitoneal injection) to induce apoptosis in hippocampal cells. The results were as follows: (1) the expression of hypoxia-inducible factor-1α was dramatically decreased during the neuroprotective time window. (2) The kainic acid-induced apoptosis in the hippocampus was significantly decreased in rats exposed to electromagnetic fields. (3) Electromagnetic fields exposure shortened the escape time in water maze test. (4) Electromagnetic fields exposure accelerated the recovery of the blood-brain barrier after brain injury. These findings revealed that extremely low-frequency electromagnetic fields significantly prolong the window of opportunity for brain protection and enhance the intensity of neuroprotection after traumatic brain injury.

  7. Very Early Administration of Progesterone for Acute Traumatic Brain Injury

    PubMed Central

    Wright, David W.; Yeatts, Sharon D.; Silbergleit, Robert; Palesch, Yuko Y.; Hertzberg, Vicki S.; Frankel, Michael; Goldstein, Felicia C.; Caveney, Angela F.; Howlett-Smith, Harriet; Bengelink, Erin M.; Manley, Geoffrey T.; Merck, Lisa H.; Janis, L. Scott; Barsan, William G.

    2015-01-01

    BACKGROUND Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Progesterone has been shown to improve neurologic outcome in multiple experimental models and two early-phase trials involving patients with TBI. METHODS We conducted a double-blind, multicenter clinical trial in which patients with severe, moderate-to-severe, or moderate acute TBI (Glasgow Coma Scale score of 4 to 12, on a scale from 3 to 15, with lower scores indicating a lower level of consciousness) were randomly assigned to intravenous progesterone or placebo, with the study treatment initiated within 4 hours after injury and administered for a total of 96 hours. Efficacy was defined as an increase of 10 percentage points in the proportion of patients with a favorable outcome, as determined with the use of the stratified dichotomy of the Extended Glasgow Outcome Scale score at 6 months after injury. Secondary outcomes included mortality and the Disability Rating Scale score. RESULTS A total of 882 of the planned sample of 1140 patients underwent randomization before the trial was stopped for futility with respect to the primary outcome. The study groups were similar with regard to baseline characteristics; the median age of the patients was 35 years, 73.7% were men, 15.2% were black, and the mean Injury Severity Score was 24.4 (on a scale from 0 to 75, with higher scores indicating greater severity). The most frequent mechanism of injury was a motor vehicle accident. There was no significant difference between the progesterone group and the placebo group in the proportion of patients with a favorable outcome (relative benefit of progesterone, 0.95; 95% confidence interval [CI], 0.85 to 1.06; P = 0.35). Phlebitis or thrombophlebitis was more frequent in the progesterone group than in the placebo group (relative risk, 3.03; CI, 1.96 to 4.66). There were no significant differences in the other prespecified safety outcomes. CONCLUSIONS This clinical trial did not show a

  8. Pathologic electrographic changes after experimental traumatic brain injury

    PubMed Central

    Bragin, Anatol; Li, Lin; Almajano, Joyel; Alvarado-Rojas, Catalina; Reid, Aylin Y.; Staba, Richard J.; Engel, Jerome

    2016-01-01

    Summary Objective To investigate possible electroencephalography (EEG) correlates of epileptogenesis after traumatic brain injury (TBI) using the fluid percussion model. Methods Experiments were conducted on adult 2- to 4-month-old male Sprague-Dawley rats. Two groups of animals were studied: (1) the TBI group with depth and screw electrodes implanted immediately after the fluid percussion injury (FPI) procedure, and (2) a naive age-matched control group with the same electrode implantation montage. Pairs of tungsten microelectrodes (50 µm outer diameter) and screw electrodes were implanted in neocortex inside the TBI core, areas adjacent to TBI, and remote areas. EEG activity, recorded on the day of FPI, and continuously for 2 weeks, was analyzed for possible electrographic biomarkers of epileptogenesis. Video-EEG monitoring was also performed continuously in the TBI group to capture electrographic and behavioral seizures until the caps came off (28–189 days), and for 1 week, at 2, 3, and 6 months of age, in the control group. Results Pathologic high-frequency oscillations (pHFOs) with a central frequency between 100 and 600 Hz, were recorded from microelectrodes, beginning during the first two post-FPI weeks, in 7 of 12 animals in the TBI group (58%) and never in the controls. pHFOs only occurred in cortical areas within or adjacent to the TBI core. These were associated with synchronous multiunit discharges and popSpikes, duration 15–40 msec. Repetitive pHFOs and EEG spikes (rHFOSs) formed paroxysmal activity, with a unique arcuate pattern, in the frequency band 10–16 Hz in the same areas as isolated pHFOs, and these events were also recorded by screw electrodes. Although loss of caps prevented long-term recordings from all rats, pHFOs and rHFOSs occurred during the first 2 weeks in all four animals that later developed seizures, and none of the rats without these events developed late seizures. Significance pHFOs, similar to those associated with

  9. Energy Drinks, Alcohol, Sports and Traumatic Brain Injuries among Adolescents

    PubMed Central

    Ilie, Gabriela; Boak, Angela; Mann, Robert E.; Adlaf, Edward M.; Hamilton, Hayley; Asbridge, Mark; Rehm, Jürgen; Cusimano, Michael D.

    2015-01-01

    Importance The high prevalence of traumatic brain injuries (TBI) among adolescents has brought much focus to this area in recent years. Sports injuries have been identified as a main mechanism. Although energy drinks, including those mixed with alcohol, are often used by young athletes and other adolescents they have not been examined in relation to TBI. Objective We report on the prevalence of adolescent TBI and its associations with energy drinks, alcohol and energy drink mixed in with alcohol consumption. Design, Settings and Participants Data were derived from the Centre for Addiction and Mental Health’s 2013 Ontario Student Drug Use and Health Survey (OSDUHS). This population-based cross-sectional school survey included 10,272 7th to 12th graders (ages 11–20) who completed anonymous self-administered questionnaires in classrooms. Main Outcome Measures Mild to severe TBI were defined as those resulting in a loss of consciousness for at least five minutes, or being hospitalized for at least one night. Mechanism of TBI, prevalence estimates of TBI, and odds of energy drink consumption, alcohol use, and consumption of energy drinks mixed with alcohol are assessed. Results Among all students, 22.4% (95% CI: 20.7, 24.1) reported a history of TBI. Sports injuries remain the main mechanism of a recent (past year) TBI (45.5%, 95% CI: 41.0, 50.1). Multinomial logistic regression showed that relative to adolescents who never sustained a TBI, the odds of sustaining a recent TBI were greater for those consuming alcohol, energy drinks, and energy drinks mixed in with alcohol than abstainers. Odds ratios were higher for these behaviors among students who sustained a recent TBI than those who sustained a former TBI (lifetime but not past 12 months). Relative to recent TBI due to other causes of injury, adolescents who sustained a recent TBI while playing sports had higher odds of recent energy drinks consumption than abstainers. Conclusions and Relevance TBI remains a

  10. [Deep Vein Thrombosis Prophylaxis in Patients with Traumatic Brain Injury].

    PubMed

    Silva, Vinícius Trindade Gomes da; Iglesio, Ricardo; Paiva, Wellingson Silva; Siqueira, Mario Gilberto; Teixeira, Manoel Jacobsen

    2015-01-01

    Introdução: O risco de trombose venosa profunda encontra-se aumentado em doentes vítimas de traumatismo cranioencefálico, mas a profilaxia da trombose venosa profunda se confronta com o possível risco de piora de lesões hemorrágicas relacionados ao traumatismo cranioencefálico. Neste artigo apresentamos uma revisão crítica do tema e propomos um protocolo de profilaxia para estes doentes.Material e Métodos: Foi realizada uma pesquisa na base de dados Medline/PubMed, Cochrane, e Scielo de janeiro de 1998 a janeiro de 2014 com a expressão de busca âÄúdeep venous thrombosis and prophylaxis and traumatic brain injuryâÄù. Foram encontrados 44 artigos usando os termos MeSH definidos. Destes foram selecionados 23 artigos, usando como critérios: publicação em inglês ou português, fase aguda do traumatismo cranioencefálico moderado e grave, profilaxia mecânica não invasiva ou química.Resultados: O traumatismo cranioencefálico é um fator de risco para trombose venosa profunda e tromboembolismo pulmonar. A chance de trombose venosa profunda é 2,59 vezes maior em doentes com traumatismo cranioencefálico. A prevalência de trombose venosa profunda e embolia pulmonar em doentes que sofreram traumatismo cranioencefálico é de 20%, podendo atingir 30% dos doentes em alguns estudos.Discussão e Conclusão: As diversas formas de traumatismo de forma isolada constituem fator de risco para trombose venosa profunda e tromboembolismo pulmonar. Ensaios clínicos são necessários para estabelecer a eficácia da profilaxia e o melhor momento de iniciar medicação para trombose venosa profunda em doentes com traumatismo craniencefálico.

  11. Visual performance and the ocular surface in traumatic brain injury.

    PubMed

    Cockerham, Glenn C; Lemke, Sonne; Glynn-Milley, Catherine; Zumhagen, Lars; Cockerham, Kimberly P

    2013-01-01

    The pathophysiology of neurotrauma is reviewed and an original study investigating the prevalence of dry eye disease in a sample of veterans with traumatic brain injury (TBI) is presented. Fifty-three veterans with TBI were evaluated by history of injury, past ocular history, and medication use. Ocular Disease Surface Index (OSDI), ocular examination, cranial nerve evaluation, tear osmolarity, tear film break-up time (TFBUT), ocular surface staining and tear production testing were performed. A matched comparison group underwent similar testing. TBI causes were blast (44) or non-blast (9). TBI subjects scored significantly worse on the OSDI (P<.001), and ocular surface staining by Oxford scale (P<.001) than non-TBI subjects. Scores for tear film breakup (P=.6), basal tear production less than 3 mm (P=.13), and tear osmolarity greater than 314 mOsm/L (P=.15) were all higher in TBI subjects; significantly more TBI subjects had at least one abnormal dry eye measure than comparisons (P<.001). The OSDI related to presence of dry eye symptoms (P<.01). These effects were present in both blast and non-blast TBI. Seventy percent of TBI subjects were taking at least one medication in the following classes: antidepressant, atypical antipsychotic, anticonvulsant, or h1-antihistamine. There was no association between any medication class and the OSDI or dry eye measures. Reduced corneal sensation in 21 TBI subjects was not associated with OSDI, tear production, or TFBUT, but did correlate with reduced tear osmolarity (P=.05). History of refractive surgery, previous contact lens wear, facial nerve weakness, or meibomian gland dysfunction was not associated with DED. In summary, we found a higher prevalence of DED in subjects with TBI, both subjectively and objectively. This effect is unrelated to medication use, and it may persist for months to years. We recommend that patients with TBI from any cause be evaluated for DED using a battery of standard testing methods described in

  12. Psychotropic Medication Use during Inpatient Rehabilitation for Traumatic Brain Injury

    PubMed Central

    Hammond, Flora M.; Barrett, Ryan S.; Shea, Timothy; Seel, Ronald T.; McAlister, Thomas W.; Kaelin, Darryl; Ryser, David; Corrigan, John D.; Cullen, Nora; Horn, Susan D.

    2015-01-01

    Objective To describe psychotropic medication administration patterns during inpatient rehabilitation for traumatic brain injury (TBI) and their relationship to patient pre-injury and injury characteristics. Design Prospective observational cohort. Setting multiple acute inpatient rehabilitation units or hospitals. Participants 2,130 individuals with TBI (complicated mild, moderate, or severe) admitted for inpatient rehabilitation. Interventions NA Main Outcome Measure(s) NA Results Most frequently administered was narcotic analgesics (72% of sample) followed by antidepressants (67%), anticonvulsants (47%), antianxiolytics (33%), hypnotics (30%), stimulants (28%), antipsychotics (25%), antiparkinson agents (25%), and miscellaneous psychotropics (18%). The psychotropic agents studied were administered to 95% of the sample with 8.5% receiving only 1 and 31.8% receiving 6 or more. Degree of psychotropic medication administration varied widely between sites. Univariate analyses indicated younger patients were more likely to receive anxiolytics, antidepressants, antiparkinson agents, stimulants, antipsychotics, and narcotic analgesics, while those older were more likely to receive anticonvulsants and miscellaneous psychotropics. Men were more likely to receive antipsychotics. All medication classes were less likely administered to Asians, and more likely to those with more severe functional impairment. Use of anticonvulsants was associated with having seizures at some point during acute care or rehabilitation stays. Narcotic analgesics were more likely for those with history of drug abuse, history of anxiety and depression (premorbid or during acute care), and severe pain during rehabilitation. Psychotropic medication administration increased rather than decreased during the course of inpatient rehabilitation in each of the medication categories except for narcotics. This observation was also true for medication administration within admission functional levels (defined

  13. Neuroprotective effect of Pycnogenol® following traumatic brain injury

    PubMed Central

    Scheff, Stephen W.; Ansari, Mubeen A.; Roberts, Kelly N.

    2012-01-01

    Traumatic brain injury (TBI) involves primary and secondary injury cascades that underlie delayed neuronal dysfunction and death. Oxidative stress is one of the most celebrated secondary injury mechanisms. A close relationship exists between levels of oxidative stress and the pathogenesis of TBI. However, other cascades, such as an increase in proinflammatory cytokines, also play important roles in the overall response to the trauma. Pharmacologic intervention, in order to be successful, requires a multifaceted approach. Naturally occurring flavonoids are unique in possessing not only tremendous free radical scavenging properties but also the ability to modulate cellular homeostasis leading to a reduction in inflammation and cell toxicity. This study evaluated the therapeutic role of Pycnogenol (PYC) a patented combinational bioflavonoid. Young adult Sprague-Dawley rats were subjected to a unilateral moderate cortical contusion and treated post injury with PYC or vehicle. At either 48 or 96h post trauma, the animals were killed and the cortex and hippocampus analyzed for changes in enzymatic and non-enzymatic oxidative stress markers. In addition, possible changes in both pre and post synaptic proteins (synapsin-1, PSD-95, drebrin, synapse associated protein 97) were analyzed. Finally, a separate cohort of animals were used to evaluate two proinflammatory cytokines (IL-6, TNF-α). Following the trauma there was a significant increase in oxidative stress in both the injured cortex and the ipsilateral hippocampus. Animals treated with PYC significantly ameliorated levels of protein carbonyls, lipid peroxidation, and protein nitration. The PYC treatment also significantly reduced the loss of key pre and post synaptic proteins with some levels in the hippocampus of PYC treated animals not significantly different from sham operated controls. Although levels of the proinflammatory cytokines were significantly elevated in both injury groups, the cohort treated with PYC

  14. Traumatic Brain Injury Alters Methionine Metabolism: Implications for Pathophysiology

    PubMed Central

    Dash, Pramod K.; Hergenroeder, Georgene W.; Jeter, Cameron B.; Choi, H. Alex; Kobori, Nobuhide; Moore, Anthony N.

    2016-01-01

    Methionine is an essential proteinogenic amino acid that is obtained from the diet. In addition to its requirement for protein biosynthesis, methionine is metabolized to generate metabolites that play key roles in a number of cellular functions. Metabolism of methionine via the transmethylation pathway generates S-adenosylmethionine (SAM) that serves as the principal methyl (−CH3) donor for DNA and histone methyltransferases (MTs) to regulate epigenetic changes in gene expression. SAM is also required for methylation of other cellular proteins that serve various functions and phosphatidylcholine synthesis that participate in cellular signaling. Under conditions of oxidative stress, homocysteine (which is derived from SAM) enters the transsulfuration pathway to generate glutathione, an important cytoprotective molecule against oxidative damage. As both experimental and clinical studies have shown that traumatic brain injury (TBI) alters DNA and histone methylation and causes oxidative stress, we examined if TBI alters the plasma levels of methionine and its metabolites in human patients. Blood samples were collected from healthy volunteers (HV; n = 20) and patients with mild TBI (mTBI; GCS > 12; n = 20) or severe TBI (sTBI; GCS < 8; n = 20) within the first 24 h of injury. The levels of methionine and its metabolites in the plasma samples were analyzed by either liquid chromatography-mass spectrometry or gas chromatography-mass spectrometry (LC-MS or GC-MS). sTBI decreased the levels of methionine, SAM, betaine and 2-methylglycine as compared to HV, indicating a decrease in metabolism through the transmethylation cycle. In addition, precursors for the generation of glutathione, cysteine and glycine were also found to be decreased as were intermediate metabolites of the gamma-glutamyl cycle (gamma-glutamyl amino acids and 5-oxoproline). mTBI also decreased the levels of methionine, α-ketobutyrate, 2 hydroxybutyrate and glycine, albeit to lesser degrees than

  15. Traumatic Brain Injury Studies in Britain during World War II.

    PubMed

    Lanska, Douglas J

    2016-01-01

    As a result of the wartime urgency to understand, prevent, and treat patients with traumatic brain injury (TBI) during World War II (WWII), clinicians and basic scientists in Great Britain collaborated on research projects that included accident investigations, epidemiologic studies, and development of animal and physical models. Very quickly, investigators from different disciplines shared information and ideas that not only led to new insights into the mechanisms of TBI but also provided very practical approaches for preventing or ameliorating at least some forms of TBI. Neurosurgeon Hugh Cairns (1896-1952) conducted a series of influential studies on the prevention and treatment of head injuries that led to recognition of a high rate of fatal TBI among motorcycle riders and subsequently to demonstrations of the utility of helmets in lowering head injury incidence and case fatality. Neurologists Derek Denny-Brown (1901-1981) and (William) Ritchie Russell (1903-1980) developed an animal model of TBI that demonstrated the fundamental importance of sudden acceleration (i.e., jerking) of the head in causing concussion and forced a distinction between head injury associated with sudden acceleration/deceleration and that associated with crush or compression. Physicist A.H.S. Holbourn (1907-1962) used theoretical arguments and simple physical models to illustrate the importance of shear stress in TBI. The work of these British neurological clinicians and scientists during WWII had a strong influence on subsequent clinical and experimental studies of TBI and also eventually resulted in effective (albeit controversial) public health campaigns and legislation in several countries to prevent head injuries among motorcycle riders and others through the use of protective helmets. Collectively, these studies accelerated our understanding of TBI and had subsequent important implications for both military and civilian populations. As a result of the wartime urgency to understand

  16. Traumatic Brain Injury Studies in Britain during World War II.

    PubMed

    Lanska, Douglas J

    2016-01-01

    As a result of the wartime urgency to understand, prevent, and treat patients with traumatic brain injury (TBI) during World War II (WWII), clinicians and basic scientists in Great Britain collaborated on research projects that included accident investigations, epidemiologic studies, and development of animal and physical models. Very quickly, investigators from different disciplines shared information and ideas that not only led to new insights into the mechanisms of TBI but also provided very practical approaches for preventing or ameliorating at least some forms of TBI. Neurosurgeon Hugh Cairns (1896-1952) conducted a series of influential studies on the prevention and treatment of head injuries that led to recognition of a high rate of fatal TBI among motorcycle riders and subsequently to demonstrations of the utility of helmets in lowering head injury incidence and case fatality. Neurologists Derek Denny-Brown (1901-1981) and (William) Ritchie Russell (1903-1980) developed an animal model of TBI that demonstrated the fundamental importance of sudden acceleration (i.e., jerking) of the head in causing concussion and forced a distinction between head injury associated with sudden acceleration/deceleration and that associated with crush or compression. Physicist A.H.S. Holbourn (1907-1962) used theoretical arguments and simple physical models to illustrate the importance of shear stress in TBI. The work of these British neurological clinicians and scientists during WWII had a strong influence on subsequent clinical and experimental studies of TBI and also eventually resulted in effective (albeit controversial) public health campaigns and legislation in several countries to prevent head injuries among motorcycle riders and others through the use of protective helmets. Collectively, these studies accelerated our understanding of TBI and had subsequent important implications for both military and civilian populations. As a result of the wartime urgency to understand

  17. Predictors of Personality Change Due to Traumatic Brain Injury in Children and Adolescents in the First Six Months after Injury.

    ERIC Educational Resources Information Center

    Max, Jeffrey E.; Levin, Harvey S.; Landis, Julie; Schachar, Russell; Saunders, Ann; Ewing-Cobbs, Linda; Chapman, Sandra B.; Dennis, Maureen

    2005-01-01

    Objective: To assess the phenomenology and predictive factors of personality change due to traumatic brain injury. Method: Children (N = 177), aged 5 to 14 years with traumatic brain injury from consecutive admissions to five trauma centers, were followed prospectively at baseline and 6 months with semistructured psychiatric interviews. Injury…

  18. Severe Traumatic Brain Injury, Frontal Lesions, and Social Aspects of Language Use: A Study of French-Speaking Adults

    ERIC Educational Resources Information Center

    Dardier, Virginie; Bernicot, Josie; Delanoe, Anaig; Vanberten, Melanie; Fayada, Catherine; Chevignard, Mathilde; Delaye, Corinne; Laurent-Vannier, Anne; Dubois, Bruno

    2011-01-01

    The purpose of this study was to gain insight into the social (pragmatic) aspects of language use by French-speaking individuals with frontal lesions following a severe traumatic brain injury. Eleven participants with traumatic brain injury performed tasks in three areas of communication: production (interview situation), comprehension (direct…

  19. Survivors of a Silent Epidemic: The Learning Experience of College Students with a History of Traumatic Brain Injury

    ERIC Educational Resources Information Center

    Schlessman, Heather A.

    2010-01-01

    A significant proportion of young adults experience a traumatic brain injury (TBI) every year, and students with this history are becoming a growing presence on college campuses. A review of the literature revealed very little research exploring the learning experiences of college students with a history of traumatic brain injury. The purpose of…

  20. Traumatic Brain Injury: General Information. Fact Sheet Number 18 = Lesion Cerebral: Informacion General. Fact Sheet Number 18.

    ERIC Educational Resources Information Center

    National Information Center for Children and Youth with Disabilities, Washington, DC.

    This fact sheet offers general information about traumatic brain injury. Information includes a definition, incidence, individual characteristics, and educational implications. The fact sheet notes that the designation of traumatic brain injury as a separate category of disability signals that schools should provide children and youth with access…