MRI analysis

Brain MRI, including T1-weighted imaging, T2-weighted imaging, fluid-attenuated inversion recovery (FLAIR), DWI, SWI, and three-dimensional time-of-flight magnetic resonance angiography (3D-TOF-MRA) was performed for each patient using a 3.0 T system (Skyra, Siemens Medical, Germany) within 24 h after admission. Axial spin-echo T1 (TR/TE/excitation = 1500/11/1, FOV = 220 mm, slice thickness/gap = 4 mm/1.2 mm, matrix = 320 × 320, time of acquisition = 1 min 26 s) and turbo spin-echo T2 (TR/TE/ excitation = 4720/96/2, turbo factor 15, FOV = 220 mm, slice thickness/gap = 4 mm/1.2 mm, matrix of 512 × 512, time of acquisition = 1 min 50 s) images were also acquired. Coronal position FLAIR (TR/TE/excitation = 9000/84/1, FOV = 230 mm, slice thickness/gap = 5 mm/1.5 mm, matrix 320 × 320, time of acquisition = 1 min 50 s) and DWI spin-echo planar imaging (EPI) (TR/TE/excitation = 4640/67/1, matrix = 192 × 192, FOV = 230 mm, slice thickness/gap = 4 mm/1.2 mm, EPI factor = 91, acquisition time = 1 min 44 s) sequences with three orthogonally applied gradients were used, with b values of 0 and 1000. SWI (TR/TE/excitation = 27/20/1, FOV = 220 mm, slice thickness/gap = 3 mm/0.6 mm, matrix 256 × 256, time of acquisition = 2 min 28 s) and 3D-TOF-MRA (TR/TE/excitation = 21/3.42/1, FOV = 200 mm, slice thickness/gap = 0.7 mm/− 0.14 mm, matrix 384 × 384, time of acquisition = 3 min 36 s) were also conducted.

An experienced neuroradiologist and a trained neurologist (WF and YKC), who were blinded to the patients’ clinical information, independently assessed the MRI variables as well as the APCVS as follows:

Infarct. The location, number, and volume of acute infarcts were examined on DWI and the total volume was calculated by multiplying the total area by the sum of the slice thickness and the gap.

White matter lesions. The severity of white matter lesions was graded using the four-point scale of Fazekas et al. [19] Deep white matter hyperintensities and periventricular hyperintensities were scored.

Intracranial arterial stenosis or occlusion. This was assessed using the WASID Criteria [16]. Symptomatic severe intracranial arterial stenosis was defined as a stenosis ≥70% that affected the ICA or the M1 segment of the MCA ipsilateral to the infarction. Intracranial large artery occlusion was defined as signal loss of distal blood flow.

Hemorrhagic transformation. This was confirmed on the basis of signal changes on T1WI, T2WI, and SWI.

APCVS. This was the result of an internal comparison of vein signals between the two hemispheres. The APCVS was defined as more and/or a larger size of cortical veins with greater signal loss on the side with SIASO than on the contralateral size without SIASO in the minimum-intensity projection of SWI (Fig. 1) [10]. Ten cases were randomly selected to test the inter-rater and intra-rater agreement, and the results indicated good agreement (inter-rater kappa 0.82; intra-rater kappa 0.86).

a Diffusion weighted imaging (DWI) in the first 24 h after admission: acute infarct in the right basal ganglia in one acute ischemic stroke patient with a National Institutes of Health Stroke Scale (NIHSS) score of 6 at admission. b Magnetic resonance angiography: occlusion in the right middle cerebral artery (MCA). c Susceptibility weighted imaging: asymmetrically prominent cortical vein sign in the right MCA territory (arrow). d Repeat DWI after early neurological deterioration (END), (Day 3 and the NIHSS score increased to 14): enlargement of the infarction