Articles: brain-injuries.
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The disturbance of normal mechanisms of oxygen delivery and metabolism is a hallmark of severe traumatic brain injury (TBI). In the past, investigations into the status of cerebral oxygen metabolism depended on changes in the differences in oxygen content between arterial and jugular venous blood. The development of jugular venous oximetry permitted continuous monitoring of jugular venous oxygen saturation, thereby overcoming earlier limitations caused by intermittent sampling. ⋯ Regional and global neuromonitoring techniques are not competitive or mutually exclusive. Rather, they are best regarded as complementary, with each providing valuable information that has a direct bearing on patient outcomes. The authors review the currently available techniques used in the monitoring of cerebral oxidative metabolism in patients who have sustained severe TBI.
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Journal of neurosurgery · Nov 2000
Clinical TrialHigh level of extracellular potassium and its correlates after severe head injury: relationship to high intracranial pressure.
Disturbed ionic and neurotransmitter homeostasis are now recognized as probably the most important mechanisms contributing to the development of secondary brain swelling after traumatic brain injury (TBI). Evidence obtained in animal models indicates that posttraumatic neuronal excitation by excitatory amino acids leads to an increase in extracellular potassium, probably due to ion channel activation. The purpose of this study was therefore to measure dialysate potassium in severely head injured patients and to correlate these results with measurements of intracranial pressure (ICP), patient outcome, and levels of dialysate glutamate and lactate, and cerebral blood flow (CBF) to determine the role of ischemia in this posttraumatic ion dysfunction. ⋯ Dialysate potassium was increased after TBI in 20% of measurements. High levels of dialysate potassium were associated with increased ICP and poor outcome. The simultaneous increase in dialysate potassium, together with dialysate glutamate and lactate, supports the concept that glutamate induces ionic flux and consequently increases ICP, which the authors speculate may be due to astrocytic swelling. Reduced CBF was also significantly correlated with increased levels of dialysate potassium. This may be due to either cell swelling or altered vasoreactivity in cerebral blood vessels caused by higher levels of potassium after trauma. Additional studies in which potassium-sensitive microelectrodes are used are needed to validate these ionic events more clearly.
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Numerous differences exist between the pediatric and adult brain-injured patient. However, children with brain injuries are frequently cared for in adult Intensive Care Units (ICUs). ⋯ The article examines the care of the brain-injured child, including monitoring, psychosocial considerations, and supportive care with emphasis on avoiding secondary brain injury by decreasing and maintaining intracranial pressure. Differences between the pediatric patients and the adult patient are highlighted throughout.
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Journal of neurosurgery · Nov 2000
Neurobehavioral protection by the neuronal calcium channel blocker ziconotide in a model of traumatic diffuse brain injury in rats.
Abnormal accumulation of intracellular calcium following traumatic brain injury (TBI) is thought to contribute to a cascade of cellular events that lead to neuropathological conditions. Therefore, the possibility that specific calcium channel antagonists might exert neuroprotective effects in TBI has been of interest. The focus of this study was to examine whether Ziconotide produces such neuroprotective effects. ⋯ These results demonstrated that the acceleration-deceleration model, which had been developed by Marmarou, et al., induces severe motor and cognitive deficits. We also demonstrated that Ziconotide exhibits substantial neuroprotective activity in this model of TBI. Improvement was observed in both motor and cognitive tasks, even though treatment was not initiated until 3 hours after injury. These findings support the development of neuronal N-type calcium channel antagonists as useful therapeutic agents in the treatment of TBI.