Acta neurochirurgica. Supplement
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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
Cerebral Arterial Time Constant Recorded from the MCA and PICA in Normal Subjects.
Cerebral arterial time constant (τ) estimates how quickly the cerebral arterial bed distal to the point of insonation is filled with arterial blood following a cardiac contraction. It is not known how τ behaves in different vascular territories in the brain. We therefore investigated the differences in τ of two cerebral arteries: the posterior inferior cerebellar artery (PICA) and the middle cerebral artery (MCA). ⋯ The MCA-supplied vascular bed has a longer distal average length, measured from the place of insonation up to the small arterioles, than the PICA-supplied vascular bed. Therefore, a longer time is needed to fill it with arterial blood volume. This study thus confirms the physiological validity of the τ concept.
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Acta Neurochir. Suppl. · Jan 2016
The Evolution of the Clinical Use of Osmotic Therapy in the Treatment of Cerebral Edema.
For almost a century, it has been known that hypertonic solutions shrink cerebral tissue. Early attempts used hypertonic solutions of ions (sodium, magnesium) and sugars (glucose, dextrose, sucrose), concentrated albumin, and, later, urea. These early attempts were largely abandoned because the effect was short lived and often followed by a period of rebound edema. ⋯ In the 1990s, use of hypertonic saline was reintroduced as an alternative to address concerns about mannitol. More recently, administration of hypertonic saline has transitioned from boluses to continuous infusions. The rationale for and data supporting the use of continuous infusions are presented.
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Acta Neurochir. Suppl. · Jan 2016
Effects of Brain Temperature on Cerebrovascular Autoregulation During the Acute Stage of Severe Traumatic Brain Injury.
The pressure reactivity index (PRx) is calculated as a moving correlation coefficient between intracranial pressure (ICP) and mean arterial blood pressure (MABP), and this analytical value is viewed as reflecting a vasomotor response to MABP variability. At present, the factors influencing the PRx value during the acute stage of traumatic brain injury (TBI) are not known. We observed significant cases where changes in the calculated value of PRx seemed to be influenced by changes in brain temperature during the course of acute stage TBI. ⋯ During the hypothermic condition, the mean value of PRx was -0.019; however, after gradual rewarming, the value of PRx increased drastically, and the mean value during the rewarming period, when the brain temperature exceeded 35 °C, was 0.331. Similarly, in another case where the patient underwent therapeutic brain hypothermia, the PRx showed a mean value of -0.038 during the hypothermic condition, and a mean value of 0.052 during the rewarming period. In both cases, a trend toward a negative correlation between ICP and MABP during brain hypothermia shifted to a positive correlation upon rewarming.