Reversed Discrepancy between CT and Diffusion-Weighted MR Imaging in Acute Ischemic Stroke
E.Y. Kima,d,
J.W. Ryooa,
H.G. Roha,
K.H. Leeb,
S.S. Kima,
I.C. Songc,
K.-H. Changc and
D.G. Nad
a Department of Radiology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
b Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
c Department of Radiology, Seoul National University College of Medicine, Seoul, Korea
d Department of Radiology, Research Institute of Radiologic Science, Yonsei University College of Medicine, Seoul, Korea
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Fig 1. Patient 7. A, ROIs for parenchymal hypoattenuation and DWI hyperintensity were placed manually on unenhanced CT and DWI (TR, 10,000 ms; TE, 71.7 ms). The 2 ROIs for CT lesion and DWI hyperintensity provide an ROI for the lesion with reversed discrepancy showing CT parenchymal hypoattenuation and no obvious DWI hyperintensity.
B, Initial unenhanced CT shows subtle hypoattenuation of lentiform nucleus, caudate, and insula in the left MCA territory (white arrows). A hyperattenuated artery sign of the left inferior M2 branch (black arrow) is also seen. Maximum intensity projection CT angiography (CTA) shows occlusion of the left inferior M2 (arrow). DWI shows hyperintense lesions in the left temporal lobe and posterior insula, but DWI hyperintensity seems very subtle and not obvious in basal ganglia and is not seen in most areas of insula. ADC map shows cytotoxic edema in the left temporal lobe. Perfusion maps show an increased TTP delay and decreased rCBF only in the left temporal lobe, and no obvious perfusion abnormality is seen in the left basal ganglia. Initial MRA shows occlusion of the left inferior M2 (arrow).
C, Follow-up MR images at day 1 show delayed DWI hyperintensity and decreased ADC in the left basal ganglia (arrow). Perfusion maps and MRA demonstrate reperfusion in the left MCA territory and recanalization of the left M2 occlusion.
D, Follow-up CT and fluid-attenuated inversion recovery (FLAIR) images (TR, 10,000 ms; TE 133 ms; TI, 2200 ms) 7 days later show infarction in the RD lesion of basal ganglia and insula, and DWI shows increased extent of DWI hyperintense lesion in the left basal ganglia. FLAIR and T2-weighted MR images (TR, 3683 ms; TE, 104 ms) obtained 9 months after the initial CT show atrophy of the left basal ganglia and insula. T1 hyperintensity is seen in the left striatum at long-term follow-up. In this patient, there was a spontaneous rapid improvement of aphasia and motor weakness within 1 hour after symptom onset.
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Fig 2. Patient 8. A, Initial unenhanced CT shows parenchymal hypoattenuation and loss of gray-white matter distinction in the left frontal lobe of ACA and MCA territory (arrows). Echo-planar spin-echo T2-weighted image (EPI T2, DWI of b value of 0, TR, 6500 ms; TE, 96.8 ms) shows no hyperintensity in the left frontal lobe. DWI (6500/96.8) and ADC map show hyperintensity and reduced ADC only in the medial frontal cortex and precentral gyrus that are only a part of hypoattenuated ischemic lesion depicted on CT. Perfusion maps show a TTP delay in the DWI lesion but no significant perfusion abnormality in the left frontal lobe lesion with reversed discrepancy on CT and DWI (arrowheads). MRA shows decreased signal intensity of the left distal MCA branches (arrow) and there was occlusion of the left A2 on MRA (not shown).
B, Follow-up MR images at day 1 show delayed DWI hyperintensity and ADC decrease in the left frontal lobe lesion with reversed discrepancy (arrows) and more severe cytotoxic edema in the medial frontal cortex and precentral gyrus of the left frontal lobe. Follow-up MRA shows recanalization of distal MCA branches but persistent perfusion abnormality in the ischemic lesion found on the initial DWI.
C, Follow-up CT image obtained 7 days after the initial CT demonstrates ischemic edema with heterogeneous hypoattenuation in the left frontal lobe. CT image obtained 11 months after the initial CT shows overt infarction with necrosis in the lesion with reversed discrepancy.
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