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Diffusion-weighted Imaging with Navigated Interleaved Echo-planar Imaging and a Conventional Gradient System1

Roland Bammer, MSc, Rudolf Stollberger, PhD, Michael Augustin, MD, Josef Simbrunner, MD, Hans Offenbacher, MD, Hendrik Kooijman, PhD, Stefan Ropele, PhD, Peter Kapeller, MD, Paul Wach, PhD, Franz Ebner, MD and Franz Fazekas, MD

1 From the Magnetic Resonance Institute (R.B., R.S., J.S., H.O., S.R., F.E., F.F.) and the Depts of Neurology (R.B., M.A., H.O., S.R., P.K., F.F.) and Radiology (J.S., F.E.), University of Graz, Auenbruggerplatz 9, A-8036 Graz, Austria; Philips Medical Systems, Hamburg, Germany (H.K.); and the Institute of Electrical and Biomedical Engineering, Graz University of Technology (P.W.). Received Feb 5, 1998; revision requested Mar 25; revision received Sep 29; accepted Nov 5. Supported in part by grants from Gemeinnützige Hertie Stiftung (R.B., S.R.) and the Faculty of Electrical Engineering, Graz University of Technology (R.B.). Address reprint requests to R.S.



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Figure 1. Acq. = acquisition, ETS = echo time shift, Gcrush = crusher gradient, GDiffusion = diffusion gradient, Gm = measurement gradient direction, Gp = phase-encoding gradient direction, Gphase = phase-encoding gradient, Gs = section-select gradient direction, Gslice = section-select gradient, RF = radio frequency, SPIR = spectral presaturation pulse. MR pulse sequence for phase-navigated DW-interleaved echo-planar imaging. The sum of the TEdiffusion and the TE can be interpreted as the TEcomposite, which is relevant for T2-weighted image contrast. To resolve the phase error caused by motion, the first echo, immediately before the second 180° pulse, was not phase encoded. The half-Fourier imaging technique was used to allow echo-planar image acquisition with a short effective TE, which led to a slight improvement in the signal-to-noise ratio and preservation of a moderate number of interleaves. It also diminished the adverse effect of motion between the navigator and imaging echo.

 


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Figure 2a. MR images of the brain obtained in a 48-year-old woman 2.5 hours after stroke onset. (a) Axial fast T2-weighted and (b) fast cerebrospinal fluid–suppressed T2-weighted images show no signal intensity changes. (c) DW image (b = 716 sec/mm2) shows a hyperintense region (arrows) in the vascular territory of the right middle cerebral artery. (d) Calculated ADC map confirms a reduction of the ADC, as indicated by the corresponding hypointense area (arrows). The mean rADC value (ie, ratio of ipsilateral ADC to contralateral ADC) was 0.605.

 


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Figure 2c. MR images of the brain obtained in a 48-year-old woman 2.5 hours after stroke onset. (a) Axial fast T2-weighted and (b) fast cerebrospinal fluid–suppressed T2-weighted images show no signal intensity changes. (c) DW image (b = 716 sec/mm2) shows a hyperintense region (arrows) in the vascular territory of the right middle cerebral artery. (d) Calculated ADC map confirms a reduction of the ADC, as indicated by the corresponding hypointense area (arrows). The mean rADC value (ie, ratio of ipsilateral ADC to contralateral ADC) was 0.605.

 


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Figure 2b. MR images of the brain obtained in a 48-year-old woman 2.5 hours after stroke onset. (a) Axial fast T2-weighted and (b) fast cerebrospinal fluid–suppressed T2-weighted images show no signal intensity changes. (c) DW image (b = 716 sec/mm2) shows a hyperintense region (arrows) in the vascular territory of the right middle cerebral artery. (d) Calculated ADC map confirms a reduction of the ADC, as indicated by the corresponding hypointense area (arrows). The mean rADC value (ie, ratio of ipsilateral ADC to contralateral ADC) was 0.605.

 


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Figure 2d. MR images of the brain obtained in a 48-year-old woman 2.5 hours after stroke onset. (a) Axial fast T2-weighted and (b) fast cerebrospinal fluid–suppressed T2-weighted images show no signal intensity changes. (c) DW image (b = 716 sec/mm2) shows a hyperintense region (arrows) in the vascular territory of the right middle cerebral artery. (d) Calculated ADC map confirms a reduction of the ADC, as indicated by the corresponding hypointense area (arrows). The mean rADC value (ie, ratio of ipsilateral ADC to contralateral ADC) was 0.605.

 


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Figure 3. DW image of the brain obtained 72 hours after stroke onset in a 62-year-old man with a small cerebellar infarction. The brain stem (arrowheads) and the cerebellar lesion (arrow) are well depicted. No substantial susceptibility artifacts are visible.

 


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Figure 4a. MR images obtained in a 75-year-old man with acute aphasia and right hemiplegia. (a) Axial T2-weighted DW-interleaved echo-planar image (b {approx} 0 sec/mm2), (b) DW image (b = 716 sec/mm2), and (c) ADC map obtained 1.5 hours after stroke onset. In b, the focal signal intensity abnormalities (arrows) around the posterior horn on the right most likely correspond to old lesions that consist of central encephalomalacia with surrounding gliosis. (c) ADC map shows no clear signs of early infarction. The darker paraventricular areas (arrowheads) resulted from anisotropy of the white matter tracts. (d–f) MR images obtained 22 hours after stroke onset. (d) Axial T2-weighted image shows diffusely increased signal intensity (arrows) in the left middle cerebral arterial territory. (e) The area of ischemic damage (arrows) is more clearly delineated on the DW image. (f) Calculated ADC map shows a reduced ADC (arrows) in the affected area (rADC = 0.297).

 


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Figure 4b. MR images obtained in a 75-year-old man with acute aphasia and right hemiplegia. (a) Axial T2-weighted DW-interleaved echo-planar image (b {approx} 0 sec/mm2), (b) DW image (b = 716 sec/mm2), and (c) ADC map obtained 1.5 hours after stroke onset. In b, the focal signal intensity abnormalities (arrows) around the posterior horn on the right most likely correspond to old lesions that consist of central encephalomalacia with surrounding gliosis. (c) ADC map shows no clear signs of early infarction. The darker paraventricular areas (arrowheads) resulted from anisotropy of the white matter tracts. (d–f) MR images obtained 22 hours after stroke onset. (d) Axial T2-weighted image shows diffusely increased signal intensity (arrows) in the left middle cerebral arterial territory. (e) The area of ischemic damage (arrows) is more clearly delineated on the DW image. (f) Calculated ADC map shows a reduced ADC (arrows) in the affected area (rADC = 0.297).

 


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Figure 4c. MR images obtained in a 75-year-old man with acute aphasia and right hemiplegia. (a) Axial T2-weighted DW-interleaved echo-planar image (b {approx} 0 sec/mm2), (b) DW image (b = 716 sec/mm2), and (c) ADC map obtained 1.5 hours after stroke onset. In b, the focal signal intensity abnormalities (arrows) around the posterior horn on the right most likely correspond to old lesions that consist of central encephalomalacia with surrounding gliosis. (c) ADC map shows no clear signs of early infarction. The darker paraventricular areas (arrowheads) resulted from anisotropy of the white matter tracts. (d–f) MR images obtained 22 hours after stroke onset. (d) Axial T2-weighted image shows diffusely increased signal intensity (arrows) in the left middle cerebral arterial territory. (e) The area of ischemic damage (arrows) is more clearly delineated on the DW image. (f) Calculated ADC map shows a reduced ADC (arrows) in the affected area (rADC = 0.297).

 


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Figure 4d. MR images obtained in a 75-year-old man with acute aphasia and right hemiplegia. (a) Axial T2-weighted DW-interleaved echo-planar image (b {approx} 0 sec/mm2), (b) DW image (b = 716 sec/mm2), and (c) ADC map obtained 1.5 hours after stroke onset. In b, the focal signal intensity abnormalities (arrows) around the posterior horn on the right most likely correspond to old lesions that consist of central encephalomalacia with surrounding gliosis. (c) ADC map shows no clear signs of early infarction. The darker paraventricular areas (arrowheads) resulted from anisotropy of the white matter tracts. (d–f) MR images obtained 22 hours after stroke onset. (d) Axial T2-weighted image shows diffusely increased signal intensity (arrows) in the left middle cerebral arterial territory. (e) The area of ischemic damage (arrows) is more clearly delineated on the DW image. (f) Calculated ADC map shows a reduced ADC (arrows) in the affected area (rADC = 0.297).

 


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Figure 4e. MR images obtained in a 75-year-old man with acute aphasia and right hemiplegia. (a) Axial T2-weighted DW-interleaved echo-planar image (b {approx} 0 sec/mm2), (b) DW image (b = 716 sec/mm2), and (c) ADC map obtained 1.5 hours after stroke onset. In b, the focal signal intensity abnormalities (arrows) around the posterior horn on the right most likely correspond to old lesions that consist of central encephalomalacia with surrounding gliosis. (c) ADC map shows no clear signs of early infarction. The darker paraventricular areas (arrowheads) resulted from anisotropy of the white matter tracts. (d–f) MR images obtained 22 hours after stroke onset. (d) Axial T2-weighted image shows diffusely increased signal intensity (arrows) in the left middle cerebral arterial territory. (e) The area of ischemic damage (arrows) is more clearly delineated on the DW image. (f) Calculated ADC map shows a reduced ADC (arrows) in the affected area (rADC = 0.297).

 


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Figure 4f. MR images obtained in a 75-year-old man with acute aphasia and right hemiplegia. (a) Axial T2-weighted DW-interleaved echo-planar image (b {approx} 0 sec/mm2), (b) DW image (b = 716 sec/mm2), and (c) ADC map obtained 1.5 hours after stroke onset. In b, the focal signal intensity abnormalities (arrows) around the posterior horn on the right most likely correspond to old lesions that consist of central encephalomalacia with surrounding gliosis. (c) ADC map shows no clear signs of early infarction. The darker paraventricular areas (arrowheads) resulted from anisotropy of the white matter tracts. (d–f) MR images obtained 22 hours after stroke onset. (d) Axial T2-weighted image shows diffusely increased signal intensity (arrows) in the left middle cerebral arterial territory. (e) The area of ischemic damage (arrows) is more clearly delineated on the DW image. (f) Calculated ADC map shows a reduced ADC (arrows) in the affected area (rADC = 0.297).

 


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Figure 5. DW images (b = 716 sec/mm2) obtained 10 days after stroke onset in a 50-year-old woman with ischemic injury in the vascular territory of the right middle and right anterior cerebral arteries. The area of acute damage has increased signal intensity and contrasts well with an old hypointense parenchymal defect (arrows) from a previous left middle cerebral arterial infarct.

 


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Figure 6. Time course of the lesions' mean rADC ({diamondsuit}). After 4–6 days of decreased mean rADCs, the values start to rise, with an increased mean rADC that is characteristic of that of old lesions. This mean rADC course contributes to the timing of infarction. Note the problem of pseudonormalization during the transitional phase.

 





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