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AJNR - American Journal of Neuroradiology

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Temporal Evolution of Diffusion after Spontaneous Supratentorial Intracranial Hemorrhage

Ayeesha K. Kamal^b, Jonathan P. Dyke^a, Jeffrey M. Katz^b, Bernardo Liberato^b, Christopher G. Filippi^a, Robert D. Zimmerman^a and Aziz M. Ulu^a

^a Department of Radiology, Weill Medical College of Cornell University, New York, NY
^b Department of Neurology & Neuroscience, Weill Medical College of Cornell University, New York, NY

View larger version (151K): [in a new window]   FIG 1. Representative example of a typical ICH. T2-weighted image (T2w), diffusion-weighted image (DWI), and diffusion constant image (Dav) are shown. The quantitative analysis that was conducted focused on whole brain diffusion (inclusive of lesion) and brain diffusion ipsilateral and contralateral to the ICH measured by region-of-interest analysis on every section (exclusive of lesion). Lesion analysis included hemorrhage and all T2-weighted surrounding abnormalities that were cored out on every section in which they were visible. Histogram shows the distribution of diffusion constants in each region of interest. Location of the mean diffusion constant (BDav) is shown.

View larger version (14K): [in a new window]   FIG 2. Whole brain diffusion after ICH. A, Whole brain diffusion is diffusely increased as early as 6 hr after supratentorial ICH. B, Increased diffusion is comparatively similar in both cerebral hemispheres ipsilateral and contralateral to the ICH.

View larger version (52K): [in a new window]   FIG 3. Temporal changes during quantitative diffusion. Comparative bar histogram shows the evolution of diffusion changes over time in this series. Whole brain diffusion of the entire group as a whole remains elevated; this effect persists even when the lesion and all surrounding edema are "cored" out. Lesion analysis shows an evolution of diffusion changes. ICH is timed from a combination of history from ictus and neuroradiologic dating. Hyperacute (<24 hr) lesions show a lower diffusion constant because the hematoma is composed of primarily solid cells with unlysed RBCs that rise to a peak during the early acute phase (1–<5 days), with maximum focal edema response. The later phase (5–<10 days) shows its greatest decrease as probably inflammatory mediated cytotoxicity maximizes. The subacute phase (10–21 days) again shows the rise of diffusivity within the lesion as cells lyse and diffusion is no longer restricted.