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Magn Reson Med Sci. 2009;8(3):121-34.

How does water diffusion in human white matter change following ischemic stroke?

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Department of Noninvasive Diagnostic Imaging, Tohoku University Graduate School of Medicine, Aoba-ku, Sendai, Japan.



Temporal evolution of the water apparent diffusion coefficients (ADC) parallel (ADC parallel) and perpendicular (ADC perpendicular) to the human white matter tract following ischemia has not been investigated systematically. We attempted to quantify the evolution of ADC parallel and ADC perpendicular and examine whether it can be interpreted by a model of ischemic edema.


We retrospectively selected 53 patients with ischemic lesions involving the posterior limb of the internal capsule (PLIC) and placed regions of interest in the right and left PLIC on ADC maps. We performed regression analysis of lesion-to-contralateral ratios of ADC parallel and ADC perpendicular against the time (t = 1-1600 h) from onset. We then fitted the estimated time courses of ADC parallel and ADC perpendicular obtained from the analysis to a model of nerve tissue composed of cylinders (axons) and spheres corresponding to isotropic structures, particularly focal cytoplasmic swellings of glial cells and axons seen in ischemic white matter.


The evolution of ADC perpendicular and ADC parallel differed. The estimated time course of ADC parallel in microm(2)*ms(-1) was 0.64 + 0.88 exp (-0.24t) for 1 < t < 54 h and 0.00059t + 0.61 for t >or= 54 h (contralateral normal value, 1.52). That of ADC perpendicular was 0.19-0.063 exp (-0.24t) for 1 < t < 54 h and 0.00040t + 0.17 for t >or=54 h (normal value 0.22). The model fitted to these values showed that the volume of the cylinders decreased, that of the spheres increased, and extracellular volume changed little from one hour to approximately one day after stroke onset.


In the human PLIC, ADC parallel continued to decrease from one hour to a few days after stroke onset, and ADC perpendicular tended to increase. The temporal evolution could be interpreted by progression of the focal cytoplasmic swelling of glial cells and axons previously observed in animal studies.

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