Aurelie Drier^1,2, Thomas Tourdias³, Igor Sibon⁴, Yohan Attal⁵, Gurkan Mutlu⁶, Stéphane Lehéricy^1,2, Yves Samson⁶, Jacques Chiras¹, Didier Dormont¹, Jean-Marc Orgogozo⁴, Vincent Dousset³, and Charlotte Rosso^6
1Neuroradiology, Pitié Salpêtrière Hospital, Paris, France, ²Centre de NeuroImagerie de Recherche - CENIR,CRICM U795, Paris, France, ³Neuroradiology, CHU Pellegrin, Bordeaux, France, ⁴Neurology, CHU Pellegrin, Bordeaux, France, ⁵CRICM, CNRS, UMR7225 équipe NEMESIS, Paris, France, ⁶Urgences cérébro-vasculaires, Pitié Salpêtrière Hospital, Paris, France

The MRI prediction of the risk of infarct growth is essential for decision making in acute stroke treatment. A method only based on DWI and ADC maps has been recently developped to identify the at-risk tissue. In this study, this new method is compared to the gold standard, the PWI/DWI mismatch. It is as efficient as the PWI/DWI mismatch for the prediction of infarct growth and more efficient for the prediction of infarct volume. The ADC-based method‘s performances are similar during and after the therapeutic window (4H30) whereas they are significantly lower after 4h30 after stroke onset with the PWI/DWI mismatch.

Lisa Willats¹, Alan Connelly^1,2, Soren Christensen^3,4, Geoffrey Donnan^2,5, Stephen Davis^4,6, and Fernando Calamante^1,2
1Brain Research Institute, Florey Neuroscience Institutes, Melbourne, Australia, ²Department of Medicine, University of Melbourne, Australia, ³Department of Radiology, University of Melbourne, Australia, ⁴Royal Melbourne Hospital, Melbourne, Australia, ⁵Florey Neuroscience Institutes, Melbourne, Australia, ⁶Department of Neurology, University of Melbourne, Australia

Recent studies have suggested that in addition to perfusion deficits, delay and dispersion (D/D) of blood flow may also increase the risk of permanent tissue damage. We investigate the infarct risk associated with D/D using generalised linear models (GLM) formed with delay insensitive global-AIF and local-AIF perfusion estimates, together with independent D/D parameters. Including D/D parameters was found to improve the GLM predictions. The global-AIF models performed better summarised over all risk thresholds. However, for a single risk threshold (as would be used clinically), the local-AIF models would perform closer to optimum for a larger proportion of patients.

Danny JJ Wang¹, David S Liebeskind¹, Qing Hao¹, Joe X Qiao², Rana Fiazv¹, Matthias Gunther^3,4, Whitney B Pope², Samuel Hou², Lirong Yan¹, Jeffrey L Saver¹, Noriko Salamon², and Jeffry R Alger^1,2
1Neurology, UCLA, Los Angeles, CA, United States, ²Radiology, UCLA, Los Angeles, CA, United States, ³Faculty of Physics and Electronics, University of Bremen, Bremen, Germany, ⁴Fraunhofer MEVIS-Institute for Medical Image Computing, Bremen, Germany

Pseudo-continuous arterial spin labeling (ASL) and dynamic susceptibility contrast enhanced (DSC) perfusion imaging were carried out in 27 cases of acute ischemic stroke. ASL CBF and DSC CBF, Tmax maps provided largely consistent results in delineating hypoperfusion lesions. ASL CBF, nevertheless, was more sensitive than DSC CBF in delineating hyperemic lesions which Tmax and MTT maps were unable to demonstrate. After calibration using CBF in control regions, a strong correlation emerged between mean ASL and DSC CBF values in the penumbral zones defined by Tmax>4s. This study illustrated the potential for combined ASL and DSC perfusion imaging in acute stroke.

Hongyu An¹, Andria L Ford², Katie D Vo³, William J Powers⁴, Jin-Moo Lee², and Weili Lin^1
1Radiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States, ²Neurology, Washington University in St. Louis, St. Louis, MO, United States,³Radiology, Washington University in St. Louis, St. Louis, MO, United States, ⁴Neurology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States

A temporal dissociation between ADC change and perfusion alterations, with ADC changes lagging behind reperfusion, was observed. Moreover, ADC recovery subsequent to reperfusion does not necessarily predict tissue salvage and it depends on whether and when reperfusion may occur.

Matus Straka¹, Heiko Schmiedeskamp¹, Greg Zaharchuk¹, Jalal B Andre¹, Jean-Marc Olivot², Nancy J Fischbein¹, Maarten G Lansberg², Michael E Moseley¹, Gregory W Albers², and Roland Bammer^1
1Radiology, Stanford University, Stanford, CA, United States, ²Stanford Stroke Center, Stanford University, Stanford, CA, United States

Typical PWI exam employs single-echo acquisitions, but accuracy of perfusion parameters from such data can be severely flawed by T1 shortening. While CBV inaccuracies are widely understood, errors in MTT are not expected as temporal parameters are assumed to be immune to these effects. We give an explanation of the problem using simulations and exemplify it on a clinical scan. We conclude that MTT can be largely underestimated if T1-effects (e.g. due to tracer leakage) are not accounted for. As a solution we present an advanced imaging scheme based on multi-echo SAGE PWI sequence that can correct these problems.

Hongyu An¹, Andria L Ford², Cihat Eldeniz¹, Yang Yang¹, Yasheng Chen¹, Katie D Vo³, William J Powers⁴, Jin-Moo Lee², and Weili Lin^1
1Radiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States, ²Neurology, Washington University in St. Louis, St. Louis, MO, United States,³Radiology, Washington University in St. Louis, St. Louis, MO, United States, ⁴Neurology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States

Tissue survival rate as a function of 3 hr and 6hr MTT prolongation revealed that distinct patterns of perfusion and subsequent perfusion changes can be utilized to separate tissue into ischemic core (MTT prolongation >15 seconds), penumbra (MTT prolongation: 5-15 seconds) and oligemia (MTT prolongation <5 seconds) using MR perfusion. Moreover, the more severely damaged tissue needs larger perfusion improvement to survive when compared to mildly injured tissue.

Nolan S Hartkamp¹, R P H Bokkers¹, H B van der Worp², M J P van Osch³, and J Hendrikse^1
1Radiology, UMC Utrecht, Utrecht, Netherlands, ²Neurology, UMC Utrecht, Utrecht, Netherlands, ³C.J. Gorter Center, Leiden UMC, Leiden, Netherlands

Lacunar infarcts are small lesions in the deep white matter, basal ganglia or brainstem. It is hypothesized that this is a manifestation of small vessel disease and that it has a different pathogenesis than cortical stroke. An association is suggested with impaired hemodynamic autoregulation. It was previously shown that steno-occlusive internal carotid artery disease leads to hemodynamic impairement of the brain. We investigate the impact of large vessel disease upon the autoregulative hemodynamics in the deep brain structures by investigating cerebrovascular reactivity in subcortical regions in patients with steno-occlusive internal carotid artery disease and compare this with healthy control subjects.

Reinoud P.H. Bokkers¹, Steven Warach², Daymara Hernandez², Matthias J van Osch³, Jeroen Hendrikse¹, Raymond V. Mirasol², José G. Merino², and Lawrence L. Latour^2
1Department of Radiology, UMCU, Utrecht, Utrecht, Netherlands, ²Section of Stroke Diagnostics and Therapeutics, NINDS, NIH, Bethesda, Maryland, United States, ³C.J. Gorter Institute for High Field MRI, LUMC, Leiden, Netherlands

The aim of our study was to test the feasibility of using arterial spin labeling (ASL) perfusion MRI for evaluating hyperacute stroke in patients where limited time is available and to evaluate the ability of ASL for detecting perfusion deficits and perfusion-diffusion mismatch as compared with dynamic susceptibility contrast (DSC) perfusion imaging. Our study shows that ASL can depict large perfusion deficits and perfusion/diffusion mismatches in correspondence with DSC and that a fast 2½ minute ASL perfusion scan may be adequate for screening patients with contraindications to gadolinium-based contrast agents.

Matus Straka¹, Bruce C Campbell², Maarten G Lansberg³, Greg Zaharchuk¹, Michael Mlynash³, Stephanie M Kemp³, Demi Thai³, Gregory W Albers³, and Roland Bammer^1
1Radiology, Stanford University, Stanford, CA, United States, ²Neurology, Royal Melbourne Hospital, Melbourne, Australia, ³Stanford Stroke Center, Stanford University, Stanford, CA, United States

Possible occurrence of secondary hemorrhage is an important consideration in stroke treatment. Based on previous research, we present a tool that can fully-automatically and in short time provide hemorrhage prediction maps based on standard DWI and PWI images. Acquired PWI data are automatically postprocessed to obtain maps cerebral blood volume (CBV) and coregistered with the DWI. The CBV maps are then mirrored about the A/P axis to obtain estimates of contralateral CBV. Hemorrhage is ultimately predicted in regions that manifest diffusion lesions together with very low CBV. An initial test on 19 stroke cases showed 83% specificity and 86% specificity.

Xihai Zhao¹, Niranjan Balu², Jinnan Wang³, Huilin Zhao⁴, Jianrong Xu⁴, and Chun Yuan^1,2
1Department of Biomedical Engineering & Center for Biomedical Imaging Research, School of Medicine, Tsinghua University, Beijing, China, People's Republic of,²Department of Radiology, University of Washington, Seattle, WA, United States, ³Philips Research North America, Briarcliff Manor, NY, United States, ⁴Department of Radiology, Renji hospital, Shanghai Jiao Tong University, Shanghai, China, People's Republic of

Multicontrast vessel wall imaging has been widely used for characterizing carotid atherosclerosis. However, this imaging protocol could not assess the full spectrum of carotid atherosclerotic lesion distribution due to its limited longitudinal coverage (40 mm). Recently, 3D fast sequence ¡®MERGE¡¯ with isotropic resolution, large-coverage (> 80 mm) and short-scan-time (2 min) is emerging as a promising approach for identification of carotid plaques. In this study, we used 3D MERGE sequence to determine carotid lesion distribution and found that near one fourth of lesions occurred in proximal common carotid artery which is beyond the imaging coverage of current multicontrast protocol.