Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2016
Measurement of Intraspinal Pressure After Spinal Cord Injury: Technical Note from the Injured Spinal Cord Pressure Evaluation Study.
Intracranial pressure (ICP) is routinely measured in patients with severe traumatic brain injury (TBI). We describe a novel technique that allowed us to monitor intraspinal pressure (ISP) at the injury site in 14 patients who had severe acute traumatic spinal cord injury (TSCI), analogous to monitoring ICP after brain injury. A Codman probe was inserted subdurally to measure the pressure of the injured spinal cord compressed against the surrounding dura. ⋯ The ISP signal characteristics after TSCI were similar to the ICP signal characteristics recorded after TBI. Importantly, there were no associated complications. Future studies are required to determine whether reducing ISP improves neurological outcome after severe TSCI.
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Acta Neurochir. Suppl. · Jan 2016
Is Impaired Autoregulation Associated with Mortality in Patients with Severe Cerebral Diseases?
Cerebral autoregulation (CA) is a mechanism that compensates for variations in cerebral perfusion pressure (CPP) by changes in cerebral blood flow resistance to keep the cerebral blood flow constant. In this study, the relationship between lethal outcome during hospitalisation and the autoregulation-related indices PRx and Mx was investigated. ⋯ Increased PRx and Mx were associated with risk of death in patients with severe cerebral diseases. The relationship with mortality was more pronounced in PRx, whereas Mx showed a better correlation with GOS score.
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Acta Neurochir. Suppl. · Jan 2016
Sevoflurane Preconditioning Confers Neuroprotection via Anti-apoptosis Effects.
Neuroprotection against cerebral ischemia afforded by volatile anesthetic preconditioning (APC) has been demonstrated both in vivo and in vitro, yet the underlying mechanism is poorly understood. We previously reported that repeated sevoflurane APC reduced infarct size in rats after focal ischemia. In this study, we investigated whether inhibition of apoptotic signaling cascades contributes to sevoflurane APC-induced neuroprotection. ⋯ APC with sevoflurane markedly decreased apoptotic cell death in rat brains, which was accompanied by decreased caspase-3 cleavage and cytochrome c release. The apoptotic suppression was associated with increased ratios of anti-apoptotic Bcl-2 family proteins over pro-apoptotic proteins and with decreased activation of JNK and p53 pathways. Thus, our data suggest that suppression of apoptotic cell death contributes to the neuroprotection against ischemic brain injury conferred by sevoflurane preconditioning.
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Acta Neurochir. Suppl. · Jan 2016
Effects of Low-Dose Unfractionated Heparin Pretreatment on Early Brain Injury after Subarachnoid Hemorrhage in Mice.
Heparin is a pleiotropic drug that antagonizes many pathophysiological mechanisms. In this study, we evaluated whether heparin prevents early brain injury (EBI) after subarachnoid hemorrhage (SAH) in mice. SAH was induced by endovascular perforation in mice randomly assigned to sham-operated (n = 8), SAH + vehicle (n = 12), SAH + 10 U heparin pretreatment (n = 11), and SAH + 30 U heparin pretreatment (n = 14) groups. ⋯ Low-dose heparin pretreatment improved neurobehavioral function, and decreased brain edema in the ipsilateral cerebral hemisphere to the perforation side. High-dose heparin had a tendency for increased SAH, which obscured the neuroprotective effects by heparin. Low-dose heparin pretreatment may decrease the development of post-SAH EBI.
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Acta Neurochir. Suppl. · Jan 2016
Plateau Waves of Intracranial Pressure and Partial Pressure of Cerebral Oxygen.
This study investigates 55 intracranial pressure (ICP) plateau waves recorded in 20 patients after severe traumatic brain injury (TBI) with a focus on a moving correlation coefficient between mean arterial pressure (ABP) and ICP, called PRx, which serves as a marker of cerebrovascular reactivity, and a moving correlation coefficient between ABP and cerebral partial pressure of oxygen (pbtO2), called ORx, which serves as a marker for cerebral oxygen reactivity. ICP and ICPamplitude increased significantly during the plateau waves, whereas CPP and pbtO2 decreased significantly. ABP, ABP amplitude, and heart rate remained unchanged. ⋯ Our data show profound cerebral vasoparalysis on top of the wave and, to a lesser extent, impairment of cerebral oxygen reactivity. The different behavior of the indices may be due to the different latencies of the cerebral blood flow and oxygen level control mechanisms. While cerebrovascular reactivity is a rapidly reacting mechanism, cerebral oxygen reactivity is slower.