Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2016
Intraventricular Injection of Noncellular Cerebrospinal Fluid from Subarachnoid Hemorrhage Patient into Rat Ventricles Leads to Ventricular Enlargement and Periventricular Injury.
Early brain injury and hydrocephalus (HCP) are important mediators of poor outcome in subarachnoid hemorrhage (SAH) patients. We aim to understand the development of HCP and subependymal cellular injury after intraventricular injection of noncellular human SAH cerebrospinal fluid (CSF) into rat ventricles. Two-hundred microliters of noncellular CSF from SAH patients or normal controls were injected into the right lateral ventricle of seven adult male Sprague-Dawley rats. ⋯ We found that the ventricular area at the bregma level in the CSF injection group was significantly larger than that in the control group (p < 0.05). The periventricular tissue in the CSF injection group had significantly more necrotic cell death as well as HO-1 expression as compared with the control group (p < 0.05). In conclusion, injection of SAH patients' CSF into the rat ventricle leads to HCP as well as subependymal injury compared with injection of control CSF.
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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
Dynamic Cerebrovascular and Intracranial Pressure Reactivity Assessment of Impaired Cerebrovascular Autoregulation in Intracranial Hypertension.
We previously suggested that the discrepancy between a critical cerebral perfusion pressure (CPP) of 30 mmHg, obtained by increasing intracranial pressure (ICP), and 60 mmHg, obtained by decreasing arterial pressure, was due to pathological microvascular shunting at high ICP [1], and that the determination of the critical CPP by the static cerebral blood flow (CBF) autoregulation curve is not valid with intracranial hypertension. Here, we demonstrated that induced dynamic ICP reactivity (iPRx), and cerebrovascular reactivity (CVRx) tests accurately identify the critical CPP in the hypertensive rat brain, which differs from that obtained by the static autoregulation curve. ⋯ At each CPP, a transient 10-mmHg increase in arterial pressure was induced by bolus intravenous dopamine. iPRx and iCVRx were calculated as ΔICP/Δ mean arterial pressure (MAP) and as ΔCBF/ΔMAP, respectively. The critical CPP at high ICP, obtained by iPRx and iCVRx, is 50 mmHg, where compromised capillary flow, transition of blood flow to nonnutritive microvascular shunts, tissue hypoxia, and brain-blood barrier leakage begin to occur, which is higher than the 30 mmHg determined by static autoregulation.