https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50288 Wed 28 Feb 2024 16:40:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24428 140 years. More widespread use of advanced clinical imaging in the past decade has led to increasing recognition of the key importance of collaterals in ischemic stroke outcome. However, recent studies from several groups indicate that failure of initially good collateral supply is a key feature of patients with delayed infarct expansion. This clinically challenging problem typically occurs in the first 1 to 2 days after hospital admission in patients with initially mild stroke symptoms. Rethrombosis of reperfused vessels was previously thought to be the likely cause of delayed infarct expansion in most patients. However, this theory is not supported by more recent evidence from imaging studies. Despite the important recent observations, there is limited understanding of the dynamic control of the collateral circulation, in particular, the cause of collateral blood flow failure. In this article, we will discuss recent observations from our experimental stroke model, indicating a dramatic increase in intracranial pressure (ICP) occurring around 24 hours after onset of even small stroke. We have also shown a significant linear reduction of collateral blood flow in response to progressive ICP elevation. We believe that a similar transient ICP elevation occurring during the first 1 to 2 days post stroke is a likely mechanism to explain delayed infarct expansion in patients with minor stroke. Perhaps surprisingly, we can find no published data on ICP at 24 hours in patients with minor stroke. The preclinical findings suggest that gathering such data should be a priority.]]> Wed 19 Jan 2022 15:18:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22101 Wed 11 Apr 2018 10:59:34 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16993 450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.]]> Wed 11 Apr 2018 09:23:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32689 Wed 10 Nov 2021 15:04:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21981 Thu 29 Nov 2018 09:37:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42159 p = 0.0001). No association was shown between sCTA weighting, collateral grade, and clinical outcome. Conclusion: sCTA weighting did not significantly impact collateral grade using three common collateral scores or their ability to predict final infarct.]]> Thu 25 Aug 2022 16:42:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48912 20, and (e) qualitative or quantitative assessment of pre-intervention collateral status on imaging using a grading scale. Random-effects meta-analysis was performed to investigate the association of aetiology with pre-intervention collateral status, and forest plots of risk ratio (RR) were generated. Results: A meta-analysis was conducted on seven studies, with a cumulative cohort of 1235 patients, to assess the association of pre-intervention collateral status with stroke aetiology. Patients with LAA were associated significantly with an increased rate of good collaterals (RR 1.24; 95% CI 1.04–1.50; p = 0.020, z = 2.33). Contrarily, CE aetiology was associated significantly with a decreased rate of good collaterals (RR 0.83; 95% CI 0.71–0.98; p = 0.027, z = −2.213). Conclusions: This study demonstrates that, in AIS patients receiving reperfusion therapy, LAA and CE aetiologies are associated significantly with collateral status.]]> Fri 14 Apr 2023 18:25:59 AEST ]]>