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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Randomized Controlled Trial Comparative Study Clinical Trial
Effect of backrest position on intracranial and cerebral perfusion pressures in traumatically brain-injured adults.
Backrest positioning for brain-injured adults is variable. Some data support using a flat backrest to optimize cerebral perfusion pressure; other data support elevating the head of the bed at least 30 degrees to reduce intracranial pressure. ⋯ The results strengthen the research foundation for raising the backrest position for adults, 18 to 45 years old, who have nonvascular, nonpenetrating, severe brain injuries.
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The evidence for post-traumatic migraine as the cause of the postconcussion syndrome in a proportion of patients is reviewed. ⋯ patients suffering recurrent post-traumatic headaches or other elements of the postconcussion syndrome should be treated for migraine.
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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.