Journal of neurotrauma
-
Journal of neurotrauma · Jan 2017
Randomized Controlled TrialVery Early Administration of Progesterone Does Not Improve Neuropsychological Outcomes in Subjects with Moderate to Severe TBI.
A Phase III, double-blind, placebo-controlled trial (ProTECT III) found that administration of progesterone did not reduce mortality or improve functional outcome as measured by the Glasgow Outcome Scale Extended (GOSE) in subjects with moderate to severe traumatic brain injury. We conducted a secondary analysis of neuropsychological outcomes to evaluate whether progesterone is associated with improved recovery of cognitive and motor functioning. ProTECT III was conducted at 49 level I trauma centers in the United States. ⋯ Analyses of covariance did not reveal significant treatment effects for memory (Buschke immediate recall, p = 0.53; delayed recall, p = 0.94), attention (Trails A speed, p = 0.81 and errors, p = 0.22; Digit Span Forward length, p = 0.66), executive functioning (Trails B speed, p = 0.97 and errors, p = 0.93; Digit Span Backward length, p = 0.60), language (timed phonemic fluency, p = 0.05), and fine motor coordination/dexterity (Grooved Pegboard dominant hand time, p = 0.75 and peg drops, p = 0.59; nondominant hand time, p = 0.74 and peg drops, p = 0.61). Pearson Product Moment Correlations demonstrated significant (p < 0.001) associations between better neuropsychological performance and higher GOSE scores. Similar to the ProTECT III trial's results of the primary outcome, the secondary outcomes do not provide evidence of a neuroprotective effect of progesterone.
-
Journal of neurotrauma · Jan 2017
Interpreting Quality of Life after Brain Injury (QOLIBRI) scores: Cross-walk with the Short Form-36.
The Quality of Life after Brain Injury (QOLIBRI) instruments are traumatic brain injury (TBI)-specific assessments of health-related quality of life (HRQoL), with established validity and reliability. The purpose of the study is to help improve the interpretability of the two QOLIBRI summary scores (the QOLIBRI Total score and the QOLBRI Overall Scale [OS] score). An analysis was conducted of 761 patients with TBI who took part in the QOLIBRI validation studies. ⋯ The percentage of cases in the sample that fell into the "impaired HRQoL" category was 36% for the Mental Component Summary, 38% for the QOLIBRI Total, and 39% for the QOLIBRI-OS. Relationships between the QOLIBRI scales and the Glasgow Outcome Scale-Extended (GOSE), as a measure of global function, are presented in the form of means and standard deviations that allow comparison with other studies, and data on age and sex are presented for the QOLIBRI-OS. While bearing in mind the potential imprecision of the comparison, the findings provide a framework for evaluating QOLIBRI summary scores in relation to generic HRQoL that improves their interpretability.
-
Journal of neurotrauma · Jan 2017
Observational StudyAugmented renal clearance (ARC) in traumatic brain injury (TBI): A single-center observational study of atrial natriuretic peptide, cardiac output, and creatinine clearance.
Augmented renal clearance (ARC) is being increasingly described in neurocritical care practice. The mechanisms driving this phenomenon are largely unknown. The aim of this project was therefore to explore changes in renal function, cardiac output (CO), and atrial natriuretic peptide (ANP) concentrations in patients with isolated traumatic brain injury (TBI). ⋯ Plasma ANP concentrations were also significantly elevated over the study period (minimum value = 243 pg/mL). These data suggest that ARC is likely to complicate the care of TBI patients with normal plasma creatinine concentrations, and may be driven by associated cardiovascular changes and/or elevated plasma ANP concentrations. However, significant additional research is required to further understand these findings.
-
Journal of neurotrauma · Jan 2017
Characterization of the ionic profile of the extracellular space of the injured and ischemic brain: A microdialysis study.
Traumatic brain injury (TBI) and ischemic stroke cause a variable disruption of ionic homeostasis and massive ionic fluxes with subsequent osmotic water movement across the cells that causes edema, brain swelling, and deformation of the damaged tissue. Although cerebral microdialysis (CMD) has been used to study the brain neurochemistry, the ionic profiles of brain interstitial space fluid have rarely been reported in humans. We studied the ionic profile in injured areas of the brain by using CMD. ⋯ In the traumatic core (TC), significantly higher levels of [Na+]o, [Cl-]o, and [K+]o were found. The main finding in the penumbra was a completely normal ionic profile for [Na+]o and [K+]o in 60% of the samples. ICP-MS coupled to ionic assays creates a powerful tool for a better understanding of the complex ionic disturbances that occur after severe TBI and ischemic stroke.
-
Journal of neurotrauma · Jan 2017
Traumatic brain injury causes endothelial dysfunction in the systemic microcirculation through arginase-1-dependent uncoupling of endothelial nitric oxide synthase.
Endothelial dysfunction is a hallmark of many chronic diseases, including diabetes and long-term hypertension. We show that acute traumatic brain injury (TBI) leads to endothelial dysfunction in rat mesenteric arteries. Endothelial-dependent dilation was greatly diminished 24 h after TBI because of impaired nitric oxide (NO) production. ⋯ Moreover, evidence for increased reactive oxygen species production, a consequence of l-arginine starvation-dependent eNOS uncoupling, was detected in endothelium and plasma. Collectively, our findings demonstrate endothelial dysfunction in a remote vascular bed after TBI, manifesting as impaired endothelial-dependent vasodilation, with increased arginase activity, decreased generation of NO, and increased O2- production. We conclude that blood vessels have a "molecular memory" of neurotrauma, 24 h after injury, because of functional changes in vascular endothelial cells; these effects are pertinent to understanding the systemic inflammatory response that occurs after TBI even in the absence of polytrauma.