“…There is uncertainty about the true nature of postinterventional cerebral hyperattenuation, specifically the extent to which postinterventional cerebral hyperattenuations correspond to hemorrhage or extravasation of iodinated contrast agent into infarcted parenchyma. [1][2][3][4] In theory, hemorrhage can be distinguished from iodinated contrast agents via MR imaging, given that blood degradation products are paramagnetic and cause specific changes on T2WI and T2 * WI, whereas iodine is diamagnetic. However, it has been shown in phantom models that at a field strength of 1.5T, side chains of iodinated contrast agents cause T1 and T2 shortening, which theoretically may mimic the imaging characteristics of intracellular methemoglobin present in early subacute intracerebral hemorrhage.…”