View clinical trials related to Traumatic Brain Injury.
Filter by:- Traumatic brain injury (TBI) is the leading cause of death and disability in people under age 45 in industrialized countries. Significant numbers of US veterans from the wars in Iraq and Afghanistan return with TBI. However, to date, there are no specific neuroprotective treatment options with proven clinical efficacy. - Erythropoietin (EPO) is approved by the FDA to treat anemia and has comprehensive preclinical data supporting its neuroprotective and neuroregenerative efficacy following traumatic (TBI) and a wide range of other acquired brain insults. Injury to small and medium-sized cerebral blood vessels is a well recognized consequence of TBI. EPO increases production of endothelial progenitor cells (EPCs) and promotes angiogenesis and neovascularization after TBI. EPO also promotes neurogenesis and improves functional recovery in animals after experimental stroke and TBI. Neovascularization is coupled with neurogenesis, and augmentation of both processes by EPO may result in lessened cognitive deficits. Neovascularization by EPO may prevent post-traumatic deficits in cerebrovascular reactivity (CVR), which can be measured noninvasively using magnetic resonance imaging (MRI). - This proposal is for a randomized, placebo-controlled pilot clinical trial designed to obtain data on the effects of EPO in humans with persistent post-concussive symptoms after TBI. The primary objective is to evaluate effect of 4 week administration of recombinant erythropoietin on numbers of circulating endothelial progenitor cells in patients with persistent symptoms during the subacute period after TBI. This information will guide the design of a future definitive study.
The purpose of this study was to study the effect of stem cell therapy on common symptoms in patients with Traumatic Brain Injury
The purpose of this study is to determine the feasibility of successfully delivering moderate intensity aerobic exercise training to depressed traumatic brain injury subjects between one and three years after injury.
Cerebral edema is seen heterogenous group of neurological disease states that mainly fall under the categories of metabolic, infectious, neoplasia, cerebrovascular, and traumatic brain injury disease states. Regardless of the driving force, cerebral edema is defined as the accumulation of fluid in the brain's intracellular and extracellular spaces. This occurs secondary to alterations in the complex interplay between four distinct fluid compartments within the cranium. In any human cranium; fluid is contained in the blood, the cerebrospinal fluid, interstitial fluid of the brain parenchyma, and the intracellular fluid of the neurons and glia. Fluid movement occurs normally between these compartments and depends on specific concentrations of solutes (such as sodium) and water. In brain-injured states, the normal regulation of this process is disturbed and cerebral edema can develop. Cerebral edema leads to increased intracranial pressure and mortality secondary to brain tissue compression, given the confines of the fixed-volume cranium. Additionally, secondary neuronal dysfunction or death can occur at the cellular level secondary to the disruption of ion gradients that control metabolism and function. While studies utilizing bolus dosing of hyperosmolar therapy to target signs or symptoms of increased intracranial pressure secondary to cerebral edema are numerous, there is a paucity of studies relating to continuous infusion of hyperosmolar therapy for targeted sustained hypernatremia for the prevention and treatment of cerebral edema. The investigators hypothesize that induced, sustained hypernatremia following traumatic brain injury will decrease the rate of cerebral edema formation and improve patient outcomes.
This investigation will explore the impact of 8 weeks of citicoline treatment on cognitive function, clinical state and substance use in 40 individuals with mild traumatic brain injury (mTBI).
Background: - Some people who have a traumatic brain injury (TBI) recover completely. Others, however, develop post-traumatic stress disorder (PTSD), with anxiety and depression. Research suggests that levels of a brain chemical called GABA may differ in people with PTSD compared to those without PTSD. Researchers want to see if TBI can affect GABA in the brain and help develop PTSD. To look at the brain, researchers will use imaging studies with the chemical 11C-Flumazenil, which will help the scan show GABA levels in the brain. Objectives: - To study the relationship between PTSD and TBI. Eligibility: The subjects will be recruited from the Walter Reed National Military Medical Center (WRNMMC). - Individuals between 18 and 50 years of age who have PTSD and/or had a mild TBI. - Healthy individuals between 18 and 50 years of age who have no history TBI and no history of PTSD. Design: - Participants will be screened with a physical exam and medical history. Urine and breath samples will also be collected. - Participants will have two imaging studies, on the same day if possible. The first will be a magnetic resonance imaging scan to look at the brain. The second will be a positron emission tomography scan with the study chemical to look at GABA pathways in the brain....
This is a placebo-controlled study intended to examine the effects of the neutraceutical citicholine, together with omega-3 fatty acids, on a range of measures in individuals with concussive head injury, often referred to as traumatic brain injury, or TBI. The study will consist of three visits, during which participants will complete brain scans, a thorough testing battery and a clinical interview to assess mood and other diagnostic information relevant to the study.
Traumatic brain injury (TBI) is a leading cause of death and disability in young people. It has been called the "signature wound" of the Iraq war because of its frequency among troops. TBI is associated with many chronic disabilities. Physical alterations include reduced exercise tolerance and profound muscle weakness, whereas psychological alterations include diminished sense of well-being, depression, fatigue and anxiety. Muscle and brain tissues rely upon circulating blood amino acids as precursors for metabolic functions. The investigators have shown that even one year after injury, plasma valine, an essential amino acid (EAA), was markedly reduced in patients with TBI compared to healthy controls. The investigators speculate that low plasma valine concentration contributes to chronic fatigue after TBI, since valine and tryptophan compete for the same transporter into the brain, and a low plasma valine concentration will allow more tryptophan to be transported. As a consequence, increased brain tryptophan will increase serotonin production, which may significantly contribute to the development of fatigue. Thus, the investigators will test if restoring valine concentration in persons with TBI may reduce fatigue perception and improve physical and neuropsychological function. Further, the investigators have previously shown that EAA intake has an anabolic effect in healthy young and elderly individuals. However, no data are currently available in persons recovering from TBI. Thus,the investigators will also test if EAA and/or valine can improve muscle mass in patients with TBI.
This open label trial is conducted to investigate the efficacy and safety of umbilical cord blood therapy for chronic traumatic brain injury patients. The study hypothesis is that the participants will show significant improvement in cognition and function after Umbilical cord blood (UCB) transplantation.
Thousands of children receive sedation for diagnostic and therapeutic interventions annually, and this number is expected to increase. Children are at higher risk for sedation-related complications than adults. In different scenarios, multiple drugs are used to achieve sedation, each one with particular adverse events that must be monitored and reported. Children that need CT scans for traumatic brain injuries often need sedation, without needing and IV line for that. Chloral hydrate is an hypnotic agent used since 1832 with low incidence of adverse events; however, despite its worldwide use, it's being abandoned due to bitter taste, long time of sedation onset, vomiting and mild sedation. Intranasal midazolam, on the other hand, produces high and fast concentrations on CSF with greater rates of success but probably with higher adverse events. There are no prospective studies with large series of patients using intranasal midazolam. The aim of this study is to determine if nasal midazolam is a safer approach and more effective sedative regimen when compared to rectal chloral hydrate to children undergoing CT scans.