Articles: brain-injuries.
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Comparative Study Clinical Trial Controlled Clinical Trial
Effect of out-of-hospital pediatric endotracheal intubation on survival and neurological outcome: a controlled clinical trial.
Endotracheal intubation (ETI) is widely used for airway management of children in the out-of-hospital setting, despite a lack of controlled trials demonstrating a positive effect on survival or neurological outcome. ⋯ These results indicate that the addition of out-of-hospital ETI to a paramedic scope of practice that already includes BVM did not improve survival or neurological outcome of pediatric patients treated in an urban EMS system.
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Traumatic brain injury is associated with a stress response that includes hyperglycemia, which has been shown to worsen neurological outcome during cerebral ischemia and hypoxia. To better examine the relationship between hyperglycemia and outcome after head injury, we studied the clinical course of 267 head-injured patients who were admitted for treatment in the neurosurgical department of Asclepeion Hospital of Athens between January 1993 and November 1997. ⋯ Early hyperglycemia is a frequent component of the stress response to head injury, a significant indicator of its severity, and a reliable predictor of outcome.
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Experimental neurology · Feb 2000
Continuous infusion of cyclosporin A postinjury significantly ameliorates cortical damage following traumatic brain injury.
Traumatic brain injury (TBI) results in the rapid necrosis of cortical tissue at the site of injury. In the ensuing hours and days, secondary injury exacerbates the original damage resulting in significant neurological dysfunction. Recent reports from our lab demonstrate that a bolus injection of the immunosuppressant cyclosporin A (CsA) is neuroprotective following TBI. ⋯ All animals receiving CsA demonstrated a significant reduction in lesion volume, with the highest dose offering the most neuroprotection (74% reduction in lesion volume). These results extend our previous findings and demonstrate that chronic infusion of CsA is neuroprotective following TBI. These findings also suggest that the mechanisms responsible for tissue necrosis following TBI are amenable to manipulation.
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Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Clinical studies have demonstrated a decline in extracellular fluid (ECF) glucose and an increase in lactate after TBI. In vitro studies suggest that this increase in lactate is mediated by increased glutamate and may provide a metabolic substrate for neurons, to aid in ionic restoration. ⋯ Furthermore, in the lactate infusion group, the dialysate glucose levels recovered to baseline levels by 4 h after injury, whereas they remained depressed through out the experiment, in the saline infusion group. We conclude that arterial lactate augmentation can increase brain dialysate lactate, and result in more rapid recovery of dialysate glucose after FPI. This may indicate a beneficial role for lactate, that may be potentially useful in the clinical situation, after TBI.
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Journal of neurotrauma · Feb 2000
Comparative StudyTemporal profile of release of neurobiochemical markers of brain damage after traumatic brain injury is associated with intracranial pathology as demonstrated in cranial computerized tomography.
This study aimed at the investigation of release patterns of neuron specific enolase (NSE) and protein S-100B after traumatic brain injury (TBI) and their association with intracranial pathologic changes as demonstrated in computerized tomography (CT). We analyzed NSE and S-100B concentrations in serial venous blood samples taken one to three days after TBI in 66 patients by the use of immunoluminometric assays. These markers are considered to be specific neurobiochemical indicators of damage to glial (S-100B) or neuronal (NSE) brain tissue. ⋯ Release patterns of S-100B and NSE differed in patients with primary cortical contusions, diffuse axonal injury (DAI), and signs of cerebral edema (ICP) without focal mass lesions. All serum concentrations of NSE and S-100B were significantly correlated with the volume of contusions. The data of the present study indicate that the early release patterns of NSE and S-100 may mirror different pathophysiological consequences of traumatic brain injury.