Journal of neurotrauma
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Journal of neurotrauma · Jun 2008
Early and sustained alterations in cerebral metabolism after traumatic brain injury in immature rats.
Although studies have shown alterations in cerebral metabolism after traumatic brain injury (TBI), clinical data in the developing brain is limited. We hypothesized that post-traumatic metabolic changes occur early (<24 h) and persist for up to 1 week. Immature rats underwent TBI to the left parietal cortex. ⋯ The NAA/Lac ratio was decreased ( approximately 15-20%) at all times (4 h, 24 h, 7 days) in the injured hemisphere of TBI rats. In conclusion, metabolic derangements begin early (<24 h) after TBI in the immature rat and are sustained for up to 7 days. Evaluation of early metabolic alterations after TBI could identify novel targets for neuroprotection in the developing brain.
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Journal of neurotrauma · Jun 2008
Fluctuations in cortical synchronization in pediatric traumatic brain injury.
Traumatic brain injury (TBI) is the leading cause of death and acquired disability in the pediatric population worldwide. We hypothesized that electroencephalography (EEG) synchrony and its temporal variability, analyzed during the acute phase following TBI, would be altered from that of normal children and as such would offer insights into TBI pathophysiology. Seventeen pediatric patients with mild to severe head injury admitted to a pediatric critical care unit were recruited along with 10 age- and gender-matched controls. ⋯ The temporal variability of phase synchronization among EEG electrodes increased as patients recovered and emerged from coma (p < 0.001). This temporal variability correlated with outcome (Pearson coefficient of 0.74) better than the worst Glasgow Coma Scale score, length of coma, or extent of injury on CT scan. This represents a novel approach in the evaluation of TBI in children.
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Journal of neurotrauma · Jun 2008
Efficacy of progesterone following a moderate unilateral cortical contusion injury.
Traumatic brain injury (TBI) results in an accumulation of edema and loss of brain tissue. Progesterone (PROG) has been reported to reduce edema and cortical tissue loss in a bilateral prefrontal cortex injury. This study tests the hypothesis that PROG is neuroprotective following a unilateral parietal cortical contusion injury (CCI). ⋯ Group IV received two additional injections (4 mg/kg on day 5; 2 mg/kg on day 6). PROG failed to alter both cortical edema and tissue sparing at any dose. Failure to modify two major sequelae associated with TBI brings into question the clinical usefulness of PROG as an effective treatment for all types of brain injury.
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Journal of neurotrauma · Jun 2008
Cerebral apoptosis in severe traumatic brain injury patients: an in vitro, in vivo, and postmortem study.
One of the most important recent observations in traumatic brain injury (TBI) relates to the potential role of apoptosis in secondary brain injury. We aimed to analyze the presence of apoptosis and the expression of apoptosis-related proteins in brain samples from patients with TBI. We also tried to find any association between the in situ results and the in vitro observations in a neuronal model of induced-apoptosis. ⋯ In vitro studies showed that apoptotic rate was an independent factor associated with mortality at 6 months (p = 0.014). In the receiving operator curve (ROC) curve, a cut-off point of 66.5% showed a sensitivity of 89.5% and specificity of 66.7% in the prediction of patients' death. Cerebral apoptosis is a prominent form of cell death in the PCZ of human traumatic cerebral contusions, and high rates of in vitro apoptosis are associated with a poorer prognosis after TBI.
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Journal of neurotrauma · Jun 2008
Effects of Glasgow Outcome Scale misclassification on traumatic brain injury clinical trials.
The Glasgow Outcome Scale (GOS) is the primary endpoint for efficacy analysis of clinical trials in traumatic brain injury (TBI). Accurate and consistent assessment of outcome after TBI is essential to the evaluation of treatment results, particularly in the context of multicenter studies and trials. The inconsistent measurement or interobserver variation on GOS outcome, or for that matter, on any outcome scales, may adversely affect the sensitivity to detect treatment effects in clinical trial. ⋯ The magnitude of such influence not only depends on the size of the misclassification, but also on the magnitude of the treatment effect. In conclusion, nondifferential misclassification directly reduces the power of finding the true treatment effect. An awareness of this procedural error and methods to reduce misclassification should be incorporated in TBI clinical trials.