Acta neurochirurgica. Supplement
-
Acta Neurochir. Suppl. · Jan 2016
Flexible Endoscopic Aspiration for Intraventricular Casting Hematoma.
Conventionally, patients suffering a massive intraventricular hemorrhage have undergone external ventricular drainage. However, long-term or repeated drainage increases the risk of complications due to infections or shunt dependency. Neuroendoscopic surgery may offer some advantages over more conventional procedures. ⋯ Early surgical intervention using a flexible endoscope and short period of post-surgical drainage can be highly effective for patients suffering from casting intraventricular hematomas associated with intracerebral hemorrhage. The advantages of this treatment may be a less invasive procedure, ICP control in the acute phase, breaking away from ventricular drainage in the early stage, and prevention of hydrocephalus or intracranial infectious complications in the long term.
-
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.
-
Acta Neurochir. Suppl. · Jan 2016
Vascular Endothelial Growth Factor in Brain Edema Formation After Subarachnoid Hemorrhage.
Vascular endothelial growth factor (VEGF) has been implicated in the pathogenesis of brain edema formation after experimental subarachnoid hemorrhage (SAH). In this study, we evaluated the effect of anti-VEGF antibody neutralization on brain edema formation after experimental SAH in mice. Mice underwent sham operation or filament puncture SAH and were assigned to sham, SAH + vehicle, or SAH + anti-VEGF antibody groups. ⋯ Anti-VEGF antibody significantly ameliorated neurological score and brain edema after SAH compared with the SAH + vehicle group. Immunohistochemistry showed that post-SAH IgG extravasation in brain tissue was suppressed by anti-VEGF antibody. This study suggests that VEGF is involved in brain edema formation after SAH, and that anti-VEGF antibody can decrease BBB permeability, suppress brain edema formation, and improve functional outcome after 24 h of SAH.
-
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.
-
We studied possible correlations between cerebral hemodynamic indices based on critical closing pressure (CrCP) and cerebrospinal fluid (CSF) compensatory dynamics, as assessed during lumbar infusion tests. Our data consisted of 34 patients with normal-pressure hydrocephalus who undertook an infusion test, in conjunction with simultaneous transcranial Doppler ultrasonography (TCD) monitoring of blood flow velocity (FV). CrCP was calculated from the monitored signals of ICP, arterial blood pressure (ABP), and FV, whereas vascular wall tension (WT) was estimated as CrCP - ICP. ⋯ CM at baseline correlated inversely with brain elasticity (R = -0.358; p = 0.038). Neither CrCP nor WT correlated with CSF compensatory parameters. Overall, CrCP increases and WT decreases during infusion tests, whereas CM at baseline pressure may act as a characterizing indicator of the cerebrospinal compensatory reserve.