Journal of neurotrauma
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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
IL-10 production is reduced by hypothermia but augmented by hyperthermia in rat microglia.
Pro-inflammatory cytokines and nitric oxide (NO) are considered responsible for exacerbating brain injury. Activated microglia produce these potentially cytotoxic factors during neuron destruction. The beneficial effects of hypothermia on neuroprotection are considered to be due, in part, to suppression of post-injury inflammatory factors by microglia. ⋯ In this study, hypothermia reduced production of IL-6, IL-10, and NO by LPS-activated microglia, suggesting that the neuroprotective effects of hypothermia might involve not only the inhibition of inflammatory factors, but also anti-inflammatory factor(s). Hyperthermia specifically increased IL-10 production in these cells. These temperature-dependent changes in IL-10 production may imply an important clinical marker for this cytokine in hypothermia-related neuronal protection and in hyperthermia-related neuronal 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
Multicenter StudyProgression of traumatic intracerebral hemorrhage: a prospective observational study.
ABSTRACT Preliminary evidence has shown that intracerebral hemorrhages, either spontaneous (sICH) or traumatic (tICH) often expand over time. An association between hemorrhage expansion and clinical outcomes has been described for sICH. The intent of this prospective, observational study was to characterize the temporal profile of hemorrhage progression, as measured by serial computed tomography (CT) scanning, with the aim of better understanding the natural course of hemorrhage progression in tICH. ⋯ This study demonstrates that tICH expansion between the baseline and 24-h CT scans occurred in approximately half of the subjects. The earlier after injury that the initial CT scan is obtained, the greater is the likelihood that the hematoma will expand on subsequent scans. The time frame during which hemorrhagic expansion occurs provides an opportunity for early intervention to limit a process with adverse prognostic implications.
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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.