Water Diffusion Compartmentation at High b Values in Ischemic Human Brain
Pierre Brugièresa,c,
Philippe Thomasa,
Anne Maravala,
Hassan Hosseinib,c,
Catherine Combesa,
Abdallah Chafiqa,
Lucile Ruela,b,c,
Stéphane Breila,b,c,
Marc Peschanskic and
André Gastona
a Department of Neuroradiology and Neurology, Créteil; Siemens SA, St Denis
b Department of Henri Mondor Hospital, Neurology, Créteil; Siemens SA, St Denis
c INSERM U421, Créteil, France
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FIG 1. Diffusion attenuation in test liquids at 22°C indicates a monoexponential signal intensity decay with the b factor.
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FIG 2. Biexponential decay curves for ROIs in the WM in healthy volunteer 8. Left, Curve fits the measured points (diamonds). Middle and right, The signal intensity (dotted line) originates from two compartments: an FDC (thin solid line) and an SDC (thick bold line). ffast represents 74.1% of the total brain water. ADCfast and ADCslow values are 125.7 x 10–5 and 13.6 x 10–5 mm2/s, respectively In C, the semi-log representation of the evolution of signal intensity with b factor shows an obvious biexponential decay.
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FIG 3. Biexponential decay of signal intensity measured in infarcted tissue (top row) and in normal contralateral WM (bottom row) in patient 4. The signal intensity (dotted line) originates from two compartments: an FDC (thin solid line) and an SDC (thick bold line). A dramatic decrease in ffast associated with increased ADCslow is observed in the infarcted tissue.
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FIG 4. Deep middle cerebral artery infarct at 72 hours after the onset of neurologic deficit in patient 9.
A and B, The infarcted parenchyma is hypointense on the global ADC map (A) and hyperintense on the fluid-attenuated inversion recovery image (B).
C, ffast parametric map shows hypointensity at the level of the infarct.
D, ADCslow parametric map shows increased ADCslow in the infarcted tissue.
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FIG 5. Temporal evolution of ffast, ADCslow (x 10–3 mm2/s), and ADCfast (x 10–3 mm3/s) in patient 8 with ischemic stroke. The maximum decrease in ffast and the maximum increase in ADCslow are observed on day 3. An initial increase in both ADCslow and ADCfast is observed on days 1 and 3. On day 5, an increase in ffast is associated with an increase in ADCfast. This could have been the consequence of rupture of the blood-brain barrier.
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FIG 6. Temporal evolution of ffast, ADCslow (x 10–3 mm2/s), and ADCfast (x 10–3 mm3/s) in patient 1 with an ischemic stroke. On day 21, ffast and ADCfast are increased when compared with values in normal WM. Normalization of ADCslow is noted on day 21.
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