Articles: brain-injuries.
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Review
Monitoring brain tissue oxymetry: will it change management of critically ill neurologic patients?
Based on the assumption that brain ischemia and hypoxia are central causes of brain damage, the maintenance of an adequate tissue oxygenation is a primary objective in the field of neurocritical care. Thus, monitoring brain tissue oxymetry, allowing the possibility to discriminate between normal and critically impaired tissue oxygenation, is recognized as an essential part of the management of the neurological critically ill patient. The clinical usefulness of this neuromonitoring tool in the area of neurosciences (traumatic brain injury, aneurysm surgery, arteriovenous malformation resection, brain tumors) is discussed. ⋯ It can also be used as a "surrogate end point" to evaluate putative therapies, targeting therapy towards improved cerebral oxygenation. As brain tissue oxygenation correlates closely with outcome, several outcome categories have been differentiated, aiding in predicting prognosis after injury. The rationale for monitoring brain tissue oxygenation is to provide essential information about oxygen supply and utilization in this specific tissue bed, thus reducing secondary brain damage and improving neurological outcome.
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In the present experiment we use a rat model of traumatic brain injury to evaluate the ability of low-pressure hyperbaric oxygen therapy (HBOT) to improve behavioral and neurobiological outcomes. The study employed an adaptation of the focal cortical contusion model. 64 Male Long-Evans rats received unilateral cortical contusion and were tested in the Morris Water Task (MWT) 31-33 days post injury. Rats were divided into three groups: an untreated control group (N=22), an HBOT treatment group (N=19) and a sham-treated normobaric air group (N=23). ⋯ The increased vascular density and improved MWT in the HBOT group were highly correlated (p<0.001). In conclusion, a 40-day series of 80 low-pressure HBOTs caused an increase in contused hippocampus vascular density and an associated improvement in cognitive function. These findings reaffirm the clinical experience of HBOT-treated patients with chronic traumatic brain injury.
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Neuroscience letters · Oct 2007
Inhibitory effect on cerebral inflammatory agents that accompany traumatic brain injury in a rat model: a potential neuroprotective mechanism of recombinant human erythropoietin (rhEPO).
Erythropoietin (EPO) has recently been shown to have a neuroprotective effect in animal models of traumatic brain injury (TBI). However, the precise mechanisms remain unclear. Cerebral inflammation plays an important role in the pathogenesis of secondary brain injury after TBI. ⋯ Measures of IL-6 showed no change after rhEPO treatment. Administration of rhEPO reduced brain edema, BBB permeability and apoptotic cells in the injured brain. In conclusion, post-TBI rhEPO administration may attenuate inflammatory response in the injured rat brain, and this may be one mechanism by which rhEPO improves outcome following TBI.
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J Neurosurg Anesthesiol · Oct 2007
Randomized Controlled TrialEffects of fentanyl and S(+)-ketamine on cerebral hemodynamics, gastrointestinal motility, and need of vasopressors in patients with intracranial pathologies: a pilot study.
In neurosurgical patients, opioids are administered to prevent secondary cerebral damage. Complications often related to the administration of opioids are a decrease in blood pressure affording the use of vasopressors and intestinal atonia. One alternative approach to opioids is the application of S(+)-ketamine. ⋯ There was no difference regarding ICP, CPP, and the time period until full enteral nutrition or first defecation between both groups. Patients who underwent analgesia with S(+)-ketamine showed a trend to a lower demand of norepinephrine compared with the fentanyl group. Our results indicate that S(+)-ketamine does not increase ICP and that its use in neurosurgical patients should not be discouraged on the basis of ICP-related concerns.
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J Neurosurg Anesthesiol · Oct 2007
Cerebral arterio-venous pCO2 difference, estimated respiratory quotient, and early posttraumatic outcome: comparison with arterio-venous lactate and oxygen differences.
Arterio-venous pCO2 difference (AVDpCO2) and estimated respiratory quotient, the ratio between AVDpCO2 and arterio-venous O2 difference, may be potentially useful estimators of irreversible posttraumatic global cerebral ischemia. Our aim was to evaluate their relevance, along with arterio-venous lactate difference (AVDL) and lactate oxygen index (LOI), in early outcome prediction. The retrospective study involved 55 patients with severe head injury, admitted consecutively in a multidisciplinary intensive care unit of a general hospital. ⋯ A multivariate model including clinical and radiologic descriptors and jugular bulb variables showed that a widening of AVDL and LOI was associated with early brain death. Whereas in the patients who died, a progressive worsening of AVDpCO2 and estimated respiratory quotient, associated with corresponding changes in AVDL and LOI were observed, in patients who survived the widening of AVDpCO2 normalized along with that of arterio-venous O2 difference. These findings suggest that the isolated measurement of widening AVDpCO2 is not specific for global cerebral ischemia, but its observation over time could be potentially more useful.