Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2016
Decreasing the Cerebral Edema Associated with Traumatic Intracerebral Hemorrhages: Use of a Minimally Invasive Technique.
Traumatic brain injury (TBI) is a major public health problem worldwide that affects all age groups. In the United States alone, there are approximately 50,000 deaths from severe traumatic brain injuries each year. In most studies, about 40 % of severe TBI have associated traumatic intracerebral hemorrhages (tICHs). ⋯ We identified eight tICHs that were treated entirely or in part with the modified Mi SPACE technique during the time period from August 15, 2014 to December 15, 2014. This modified technique was readily deployed safely and efficaciously with significant removal of the tICH as demonstrated by postoperative CT scans. The removal of tICH using this minimally invasive technique may help with the control of ICP and cerebral edema.
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Acta Neurochir. Suppl. · Jan 2016
Artefact in Physiological Data Collected from Patients with Brain Injury: Quantifying the Problem and Providing a Solution Using a Factorial Switching Linear Dynamical Systems Approach.
High-resolution, artefact-free and accurately annotated physiological data are desirable in patients with brain injury both to inform clinical decision-making and for intelligent analysis of the data in applications such as predictive modelling. We have quantified the quality of annotation surrounding artefactual events and propose a factorial switching linear dynamical systems (FSLDS) approach to automatically detect artefact in physiological data collected in the neurological intensive care unit (NICU). ⋯ The influence of artefact on physiological data collected in the NICU is a significant problem. This pilot study using an FSLDS approach shows real promise and is under further development.
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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.
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Research suggests that early brain injury following subarachnoid hemorrhage (SAH) is a primary therapeutic target, and early SAH-induced basal ganglia injury is not well studied. The present study examined basal ganglia injury in a rat model of SAH. Adult male Sprague-Dawley rats (n = 78) weighing 275-300 g underwent endovascular perforation to mimic aneurysmal SAH. ⋯ Basal ganglia neuronal injury was also determined by examining the levels of dopamine- and cAMP-regulated phosphoprotein, Mr 32 kDa (DARPP-32). We found that rats with hydrocephalus had more severe basal ganglia injury with greater DARPP-32 depletion (DARPP-32/beta-actin: 0.38 ± 0.32 vs. 0.86 ± 0.45 in rats without hydrocephalus and 1.10 ± 0.28 in sham, p < 0.05). In conclusion, SAH resulted in severe basal ganglia damage, which is associated with hydrocephalus development.
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Acta Neurochir. Suppl. · Jan 2016
Early Changes in Brain Oxygen Tension May Predict Outcome Following Severe Traumatic Brain Injury.
We report on the change in brain oxygen tension (PbtO2) over the first 24 h of monitoring in a series of 25 patients with severe traumatic brain injury (TBI) and relate this to outcome. The trend in PbtO2 for the whole group was to increase with time (mean PbtO2 17.4 [1.75] vs 24.7 [1.60] mmHg, first- vs last-hour data, respectively; p = 0.002). However, a significant increase in PbtO2 occurred in only 17 patients (68 %), all surviving to intensive care unit discharge (p = 0.006). ⋯ The cumulative length of time that PbtO2 was <20 mmHg was not significantly different among these three groups. In conclusion, although for the cohort as a whole PbtO2 increased over the first 24 h, the individual trends of PbtO2 were related to outcome. There was a significant association between improving PbtO2 and survival, despite these patients having cumulative durations of hypoxia similar to those of non-survivors.