Articles: brain-injuries.
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Journal of neurosurgery · Mar 2013
Randomized Controlled TrialEffect of rosuvastatin on cytokines after traumatic head injury.
The favorable effect of statin treatment after traumatic brain injury (TBI) has been shown in animal studies and is probably true in humans as well. The objective of this study was to determine whether acute statin treatment following TBI could reduce inflammatory cytokines and improve functional outcomes in humans. ⋯ The authors' data suggest that statins may induce an antiinflammatory effect and may promote recovery after TBI. The role of statins in TBI therapy should be confirmed in larger clinical trials.
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Undersea Hyperbar M · Mar 2013
Randomized Controlled TrialA prospective trial of hyperbaric oxygen for chronic sequelae after brain injury (HYBOBI).
Some practitioners advocate hyperbaric oxygen (HBO2) for sequelae following brain injury. This study assessed recruitment, tolerance and safety in preparation for a randomized clinical trial. ⋯ Conducting an HBO2 clinical trial in this population was feasible. Although many participants reported improvement, the lack of concurrent controls limits the strength of inferences from this trial, especially considering lack of change in standardized testing. The clinical relevance of neuroimaging changes is unknown. The findings of this study may indicate a need for caution when considering the broad application of HBO2 more than one year after brain injury due to stroke, severe TBI and anoxia, until there is more compelling evidence from carefully designed sham-controlled, blinded clinical trials.
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Randomized Controlled Trial
Effects of trauma, hemorrhage and resuscitation in aged rats.
Traumatic brain injury (TBI) is a leading cause of death in the elderly and the incidence of mortality and morbidity increases with age. This study tested the hypothesis that, after TBI followed by hemorrhagic hypotension (HH) and resuscitation, cerebral blood flow (CBF) would decrease more in aged compared with young rats. Young adult (4-6 months) and aged (20-24 months) male Sprague-Dawley rats were anesthetized with isoflurane, prepared for parasagittal fluid percussion injury (FPI) and randomly assigned to receive either moderate FPI (2.0 atm) only, moderate FPI+severe HH (40 mm Hg for 45 min) followed by return of shed blood, or sham FPI. ⋯ Despite differences in post-resuscitation MAP and CBF, there were no differences in the numbers of FJ-positive neurons in aged compared to young rats after FPI, HH and blood resuscitation. Although cerebral hypoperfusion in the aged rats was not associated with increased hippocampal cell injury, the trauma-induced reductions in CBF and post-resuscitation blood pressure may have resulted in damage to brain regions that were not examined or neurological or behavioral impairments that were not assessed in this study. Therefore, the maintenance of normal blood pressure and cerebral perfusion would be advisable in the treatment of elderly patients after TBI.
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Eur Rev Med Pharmaco · Feb 2013
Randomized Controlled TrialReliability of calcium-binding protein S100B measurement toward optimization of hyperosmolal therapy in traumatic brain injury.
Osmotherapy is a cornerstone for the management of severe Traumatic Brain Injury (TBI). Hypertonic saline (HTS) has advantages as being preferred osmotic agent, but there is inadequte knowledge regarding dose and its saftey in comparison to mannitol. S100B, as a specific neuroinflammatory biomarker in TBI might be a reliable therapeutic index following osmotic therapy. ⋯ S100B is closely related to the pathophysiological mechanism in TBI and may be useful as a therapeutic tool for treatment monitoring in TBI patients HTS is a safe and effective osmotic agent in TBI setting.
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Randomized Controlled Trial
Etanercept attenuates traumatic brain injury in rats by reducing early microglial expression of tumor necrosis factor-α.
Tumor necrosis factor-alpha (TNF-α) is elevated early in injured brain after traumatic brain injury (TBI), in humans and in animals. Etanercept (a TNF-α antagonist with anti-inflammatory effects) attenuates TBI in rats by reducing both microglial and astrocytic activation and increased serum levels of TNF-α. However, it is not known whether etanercept improves outcomes of TBI by attenuating microglia-associated, astrocytes-associated, and/or neurons-associated TNF-α expression in ischemic brain. A well clinically relevant rat model, where a lateral fluid percussion is combined with systemic administration of etanercept immediately after TBI, was used. The neurological severity score and motor function was measured on all rats preinjury and on day 3 after etanercept administration. At the same time, the neuronal and glial production of TNF-α was measured by Immunofluorescence staining. In addition, TNFα contents of ischemic cerebral homogenates was measured using commercial enzyme-linked immunosorbent assay kits. ⋯ This finding indicates that early microglia overproduction of TNF-α in the injured brain region after TBI contributes to cerebral ischemia and neurological motor deficits, which can be attenuated by etanercept therapy. Studies in this model could provide insight into the mechanisms underlying neurological motor disturbance in brain-injured patients.