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Severe Traumatic Brain Injury clinical trials

View clinical trials related to Severe Traumatic Brain Injury.

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NCT ID: NCT05566431 Recruiting - Clinical trials for Severe Traumatic Brain Injury

Benchmark Evidence Led by Latin America: Trial of Intracranial Pressure - Pediatrics

BELA TRIPP
Start date: March 22, 2023
Phase: N/A
Study type: Interventional

Narrative: Worldwide, traumatic brain injury (TBI) is a leading cause of death and disability among children and adolescents. The Investigators aim to test whether pediatric TBI treatment guided by invasive intracranial pressure monitoring produces better patient outcomes than care guided by a protocol without invasive monitoring. Study findings will inform clinical practice in treating pediatric severe TBI globally. Focused didactic and experience-based learning opportunities will increase the research capacity of pediatric intensivists in Latin America.

NCT ID: NCT04597879 Recruiting - Trauma Clinical Trials

Impact of Severe Brain Injury on Neuro-vascular and Endothelial Regulation of Peripheral Microcirculation.

MicroTC
Start date: August 1, 2021
Phase:
Study type: Observational

Severe brain injury (SBI) is one of the world's leading causes of death and disability in young adults, but its peripheral vascular consequences in humans are poorly understood. This prospective, monocentric, pathophysiological study aims to investigate differences in vasoreactivity in the anterior aspect of the contralateral forearm at the most injured cerebral hemisphere between patients with severe head trauma and patients with severe trauma without associated brain injury matched on sex and age (+/- 5 years).

NCT ID: NCT03659006 Recruiting - Clinical trials for Severe Traumatic Brain Injury

Identification of Predictive Neuroinflammatory Biomarkers of Neuro-radiological Evolution in Severe Traumatic Brain Injury

ICON-TBI
Start date: October 15, 2018
Phase: N/A
Study type: Interventional

Tertiary lesions responsible of the neurological decline after severe traumatic brain injury (TBI) are partially due to a persistent neuro-inflammation directly modulated by inflammatory mediators during the acute phase and detectable by using both multimodal MRI imaging and biological biomarkers during the acute phase after traumatic brain injury. The main objective is to identify if the level of IL-1beta in cerebrospinal fluid predict in a reliable and reproducible way, the neuro-radiological evolution evaluated by the comparison of a quantitative MRI performed in post-resuscitation and at one year (quantitative ΔIRM) in traumatic brain injuried patients. The secondary objectives are: - To understand the links between the acute and chronic neuro-inflammatory phase in a population of TBI, - To explore the contribution of the adaptive immune response in the persistent activation of the immune response, - To Examine the links between persistent neuroinflammation, clinical deterioration and neuroimaging, - To establish a correlation between the pathology and the physio-pathology of TBI.

NCT ID: NCT00788723 Recruiting - Clinical trials for Subarachnoid Hemorrhage

Cortical Excitability in Patients With Severe Brain Injury

Start date: July 2008
Phase: N/A
Study type: Interventional

The aim of the study is to evaluate the cortical excitability in the severe brain injured patients. We hypothesize that: 1. There is a continuous decrease in intracortical inhibition from healthy subjects to awake patients with severe brain injury, and to patients with impaired consciousness. 2. Decreased intracortical inhibition correlate with the degree of impairment assessed with the clinical scores in patients with severe brain injury.

NCT ID: NCT00489892 Recruiting - Clinical trials for Traumatic Brain Injury

Efficacy of Pharmacological Treatment of Working Memory Impairment After Traumatic Brain Injury: Evaluation With fMRI

Start date: August 2003
Phase: N/A
Study type: Interventional

This study is designed to examine the effects of a wake-promoting agent (Modafinil) on working memory (WM) in persons with moderate to severe TBI utilizing a double blinded placebo controlled methodology. Our approach is to evaluate participants with BOLD fMRI and a limited neuropsychological battery to examine WM performance before and after pharmacological intervention. Hypotheses 1. Because increased cognitive effort (as a function of decreased efficiency after TBI) is presumed to underlie fMRI activation dispersion that is seen during central executive WM tasks, we anticipate an attenuation of cerebral activation in prefrontal cortex during pharmacological intervention with Modafinil when compared to placebo administration on the mPASAT and vigilance testing. 2. There will be a correlation between the decreased dispersion of the fMRI signal on scans and improvement in neuropsychological measures when individuals are on Modafinil that is not seen when they are taking placebo.