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. 2001 Jun-Jul;22(6):1021-9.

Fluid-attenuated inversion recovery intraarterial signal: an early sign of hyperacute cerebral ischemia

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Fluid-attenuated inversion recovery intraarterial signal: an early sign of hyperacute cerebral ischemia

K Toyoda et al. AJNR Am J Neuroradiol. 2001 Jun-Jul.

Abstract

Background and purpose: Early detection of arterial occlusion and perfusion abnormality is necessary for effective therapy of hyperacute cerebral ischemia. We attempted to assess the utility of the fast fluid-attenuated inversion recovery (fast-FLAIR) sequence in detecting occluded arteries as high signal (referred to as intraarterial signal) and to establish the role of fast-FLAIR in detecting ischemic penumbra of hyperacute stroke within 24 hours after ictus.

Methods: We studied 60 patients with hyperacute cerebral ischemia caused by occlusion of intracranial major arteries. We compared intraarterial signal on FLAIR images with time of flight (TOF) on MR angiograms, flow voids on T2-weighted images, hyperintense lesions on diffusion-weighted images, and results of follow-up CT or MR scans.

Results: In 58 (96.7%) patients, FLAIR detected intraarterial signals as early as 35 minutes after stroke onset. In 48 (80.0%) patients, intraarterial signal on FLAIR images coincided with lack of TOF on MR angiograms. In 41 (74.5%) of 55 patients, the intraarterial signals of fast T2-weighted imaging depicted occlusion better than did deficient flow void on T2-weighted images. In 25 (41.7%) of 60 patients, the area of intraarterial signal distribution was larger than the hyperintense lesion measured on diffusion-weighted images. Areas of final infarction had sizes between those of intraarterial signal distribution on FLAIR images and lesions measured on diffusion-weighted images. In 35 (87.5%) of 40 patients, areas of intraarterial signal distribution were equal to regions of abnormal perfusion.

Conclusion: Intraarterial signal on FLAIR images is an early sign of occlusion of major arteries. FLAIR combined with diffusion-weighted imaging can be helpful to predict an area at risk for infarction (ischemic penumbra). FLAIR plays an important role for determining whether a patient should undergo perfusion study.

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Figures

<sc>fig</sc> 1.
fig 1.
A 78-year-old woman who underwent imaging 35 minutes after onset of right hemiparesis and aphasia. A and B, FLAIR images (8000/10/1 [TR/TE/excitation]), TI = 2000) show contiguous intraarterial signal, which is hyperintense to cerebral parenchyma in M1, M2, and M3 segments of the left middle cerebral artery (arrows). C, MR angiogram (32/6.8, flip angle = 15 degrees) shows corresponding lack of TOF effect in M1, M2, and M3 segments of the left middle cerebral artery. D, Diffusion-weighted image (500/123/1, b = 1200) shows faintly hyperintense lesion localized in the area fed by left lateral lenticulostriate artery (arrow); however, there is no change in the hemispheric territory of the left middle cerebral artery. E, Postcontrast MR angiogram (32/6.8, flip angle = 15 degrees) shows intraluminal enhancement in the left middle cerebral artery except for in the distal potion of the M1 segment. Arrow indicates complete obstruction in distal portion of left M1 segment. F, T2-weighted image (4500/96/1) obtained 7 days after onset confirmed final infarction is in the entire territory of the left middle cerebral artery. Note the diffusion-weighted lesion is still smaller than the area of intraarterial signal distribution. Intraarterial signal consists of not only complete obstruction but also slow flow. The area of final infarct corresponds to the area of intraarterial signal distribution.
<sc>fig</sc> 2.
fig 2.
A 71-year-old woman who underwent imaging 7 hours after onset of right hemiparesis and aphasia. A and B, FLAIR images (8000/10/1, TI = 2000) show intraarterial signal in M1, M2, and M3 segments of the left middle cerebral artery (arrows). C, MR angiogram (32/6.8, flip angle = 15 degree) demonstrates lack of TOF in the left internal carotid and middle cerebral arteries. Perfusion imaging (not shown) showed a hypoperfused area with increased time-to-peak and mean transit time values in the left middle cerebral artery territory as large as the area of intraarterial signal distribution and lack of TOF. D, Diffusion-weighted image (500/123/1, b = 1200) shows hyperintense lesion in the left basal ganglia and insular cortex. E, Postcontrast MR angiogram (32/6.8, flip angle = 15 degrees) shows intraluminal enhancement in the left middle cerebral artery except for in the M1 segment. Arrow indicates complete obstruction in the left M1 segment. F, Final infarction is confirmed in the basal ganglia and insular cortex by CT performed 9 days after stroke symptom onset, corresponding to the initial lesion seen on diffusion-weighted images. Note lesion in D is smaller than the area of intraarterial signal distribution. Intraarterial signal consists of not only complete obstruction but also slow collateral circulation. The area of final infarct is smaller than that of intraarterial signal distribution. Ischemic penumbra may be present in the mismatch between the intraarterial signal distribution and the diffusion-weighted lesion.
<sc>fig</sc> 3.
fig 3.
A 59-year-old man who presented with homonymous hemianopsia. MR imaging was performed 13 hours after stroke symptom onset. A, MR angiogram (32/6.8, flip angle = 15 degrees) shows lack of TOF in the right posterior communicating artery. B, On FLAIR images (8000/10/1, TI= 2000), intraarterial signal is visible in the right posterior cerebral artery (arrow); however, signal is discontinuous and isointense to cerebral parenchyma. Final infarction was confirmed in the posterior cerebral territory on T2-weighted image (not shown) obtained 14 days after stroke symptom onset. Note that FLAIR is inferior to MR angiography in detecting occluded artery.
<sc>fig</sc> 4.
fig 4.
An 83-year-old woman who underwent imaging 23.5 hours after onset of loss of consciousness. A, MR angiogram (32/6.8, flip angle = 15 degree) shows occlusion in distal portion of M1 segment of the right middle cerebral artery. B, FLAIR image (8000/10/1, TI = 2000) already shows hyperintense lesion and cortical swelling in the right middle cerebral artery territory. Intraarterial signal (arrows) is shown in the right middle cerebral artery corresponding to lack of TOF; however, signal is hampered by narrowed sulci owing to vasogenic edema.
<sc>fig</sc> 5.
fig 5.
A 62-year-old man who underwent imaging 2.5 hours after onset of loss of consciousness and left hemiparesis. A and B, FLAIR images (8000/10/1, TI = 2000) show intraarterial signal in the M1 (arrows), M2 (arrowheads), and M3 (thin long arrows) segments of the right middle cerebral artery. Old infarction proceeds in the right insular cortex. C and D (same level as in A and B), T2-weighted images (4500/96/1) show lack of flow void in M1 (arrows) and M2 (arrowheads) segments; however, evidence of flow void is visible in the M3 segment (thin long arrows). MR angiogram (not shown) shows lack of TOF in the right middle cerebral artery. CT confirmed final infarction in both perforator and hemispheric-branch territories of the right middle cerebral artery.

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References

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