High Temporal Resolution Diffusion MRI of Global Cerebral Ischemia and Reperfusion

Journal of Cerebral Blood Flow and Metabolism - Tập 16 Số 5 - Trang 892-905 - 1996
Carlo Pierpaoli1, Jeffry R. Alger2,1, Andrea Righini1, James Mattiello3, Russell R. Dickerson1, Daryl Des Pres4, Alan Barnett1, Giovanni Di Chiro1
1Neuroimaging Branch, National Institute of Neurological Diseases and Stroke
2Department of Radiological Sciences, UCLA, Los Angeles, California, U.S.A.
3Biomedical Engineering and Instrumentation Program, Bethesda, Maryland
4In Vivo NMR Center, NCRR, National Institutes of Health, Bethesda, Maryland

Tóm tắt

Although brain ischemia has been extensively studied using diffusion-weighted magnetic resonance imaging, most studies performed so far have not had adequate time resolution to follow the temporal changes in the water apparent diffusion coefficient (ADC) in hyperacute ischemia. Using diffusion echo planar imaging, we obtained ADC maps (calculated from measurements made with 8 b-values) with a time resolution of 43 s in a feline model of global brain ischemia and reperfusion. Different protocols were performed: 10-min hypoperfusion, 10- and 22-min ischemia followed by reperfusion, and cardiac arrest. ADC values were obtained from white matter of the internal capsule and from the thalamus. Cortical gray matter measurements were not deemed reliable due to the close proximity of CSF in the cortical sulci. Following occlusion, the ADC declined in the thalamus to <2 SD of its normal baseline value within 1.5–2.5 min. This decay was exponential with a time constant (τ ± SD) of 6.0 ± 2.6 min; no further decrease in the ADC was observed 10 min following ischemia. Following reperfusion, in animals that showed ADC recovery, the ADC began increasing immediately, returning to its preischemic value in ∼15 min. No significant ADC changes were observed during hypoperfusion. Following cardiac arrest, the decay of ADC was more rapid in the thalamus (τ = 2.6 ± 0.6 min) than in white matter (τ = 6.6 ± 1.8 min). We observed that the ADC at 40 min after cardiac arrest was similar to the ADC at 10 min after ischemia. Given that all animals subjected to 10-min ischemic episodes showed ADC recovery with reperfusion, doubt is cast on whether it is possible to define a threshold value of the ADC below which brain tissue is irreversibly damaged. Finally, despite variability in the time constants of the ADC decay induced by ischemia, the ADC values at 10 min were very similar in all the animals. This suggests that when blood flow is diminished sufficiently to induce an ADC reduction, differences in perfusion affect the rapidity of the decrease but not the final asymptotic value reached.

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Journal of Cerebral Blood Flow and Metabolism

Tập 16 Số 5

892-905

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