London, United Kingdom 2013 3 Experimental studies Reliability of the CT perfusion cerebral blood volume parameter in acute ischemic stroke C.D. d’Esterre1, T.Y. Lee2, S. Ceruti3, G. Roversi4, A. Saletti5, E. Fainardi6 Western University, London, CANADA1, Western University, Lawson Health Research, Robarts Research Institute, London, CANADA2, 3Neuroradiology Unit, Department of Neurosciences and Rehabilitation, Azienda Ospedaliero-Universitaria, Ferrara, ITALY3, 4Section of Neurology, Depart-ment of Medical and Surgical Sciences of the Communication and Behaviour, University of Ferrara, Ferrara, ITALY4, 3Neuroradiology Unit, Department of Neurosciences and Rehabilitation, Azienda Ospedaliero-Universitaria, Ferrara, ITALY5, 3Neuroradiology Unit, Department of Neurosciences and Rehabilitation, Azienda Ospedaliero-Universitaria, Ferrara, ITALY6 Introduction:Recent evidence suggests that the CBV parameter is unreliable during the acute isch-emic stroke (AIS) setting. We investigate the physiological and technical variables affecting the reli-ability of the CBV parameter in assessing infarct in AIS. Methods:Sixty-four patients were enrolled. Four 50s duration CTP studies were acquired at <6 hours, 24-hr, 7-day and 3-month. Recanalization at 24-hrs, NIHSS at each time point, and severity of hemorrhagic transformation (HT) were determined. The agreement between the admission CBV defect volume (CBVD) and final infarct volume on 3-month NCCT (NCCTD) was assessed with Bland-Altman and Pearson correlation analysis for recanalization positive and negative groups and sub-groups based on truncation of the ischemic time-density curve (ITDC) and hypervolemia status at admission (Table). Also, NCCTD was superimposed onto the CBV and CBF functional maps to obtain parameter values at each time point. Results:The 95% limits of agreement between CBVD and NCCTD were widest for the recanali-zation negative group. Patients with recanalization and no truncation had the highest correlation (R=0.81) and regression slope (0.80) between CBVD and NCCTD. Regression slopes were sig-nificantly lower for patients with admission hypervolemia with/out recanalization. Admission CBVD volume and very low gray and white matter CBF and CBV values were associated with HT (p<0.05). 83% of hypervolemic tissue at admission (CBF/CBV mismatch) and 24 hours (either a matched increase or mismatch in CBF/CBV) became infarcted. Conclusion:Late hypervolemia/hyperperfusion was not associated with clinical decline or HAT, but could mask late evolving infarction (Figure 1A). Early hypervolemia, as seen in the CBF/CBV mis-match, could contain ‘hidden infarction’ due to opening of non-nutritive arteriovenous shunts caus-ing venous filling (Figure 1B). Very low CBV, or a matched decrease in CBF/CBV, remains a valu-able predictor of infarct core, and potentially HAT. E-Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 247 2 Experimental studies The effects of intravenous immunoglobulin (IVIg) on the blood-brain barrier integrity after ischemic stroke-induced brain injury A. Widiapradja1, T. Santro2, S. Manzanero3, T. V. Arumugam4 The University of Queensland, Brisbane, AUSTRALIA1, The University of Queensland, Bris-bane, AUSTRALIA2, The University of Queensland, Brisbane, AUSTRALIA3, The University of Queensland, Brisbane, AUSTRALIA4 Background: Stroke is the second leading cause of death worldwide. The molecular mechanisms that occur during the ischemic insult greatly disrupt the integrity of the blood-brain barrier (BBB) resulting in an increase in its permeability, and the subsequent infiltration of leukocytes that exacer-bate the injury. Intravenous immunoglobulin (IVIg) has been shown to be able to elicit neuroprotec-tion by altering the neuronal cell death pathways, reducing the activation of glial cells and the tran-sendothelial migration of leukocytes into the site of injury. However, the mechanism on how IVIg limits BBB breakdown still remains elusive. This project investigates the effects of IVIg on BBB integrity in ischemic stroke-induced brain injury in both in vitro and in vivo. Methods: Immunoblotting and immunofluorescence are performed in order to observe and quantify the level of tight junction proteins in IVIg treated murine brain endothelial cells (bEnd3) subject-ed to oxygen and glucose deprivation (n=6), and IVIg treated murine brain tissue following isch-emic- induced stroke (n=8). Observation of leukocyte infiltration in IVIg-treated mice following ischemic stroke is done through intravital microscopy. Results: Immunoblotting shows the expression of the tight junction proteins such as occludin and claudin5 are significantly increased in IVIg-treated samples in both in vitro and in vivo. In addition, zona occludin 1, which binds to occludin and claudin5 is also increased (p=0.012). Intravital micros-copy shows reduced leukocyte infiltration into the site of injury in IVIg-treated mice following isch-emic stroke. Conclusion: IVIg has shown to be able to improve BBB integrity following ischemic brain injury by elevating the level of tight junction proteins, hence reducing leukocyte infiltration into the site of injury. These results indicate that IVIg is able to strengthen the integrity of the BBB following isch-emic stroke.
Karger_ESC London_2013
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