The appearance of intracranial hemorrhage at magnetic resonance (MR) imaging depends primarily on the age of the hematoma and the type of MR contrast (ie, T1 or T2 weighted). As a hematoma ages, the hemoglobin passes through several forms (oxyhemoglobin, deoxyhemoglobin, and methemoglobin) prior to red cell lysis and breakdown into ferritin and hemosiderin. Five distinct stages of hemorrhage can be defined: hyperacute (intracellular oxyhemoglobin, long T1 and T2), acute (intracellular deoxyhemoglobin, long T1, short T2), early subacute (intracellular methemoglobin, short T1, short T2), late subacute (extracellular methemoglobin, short T1, long T2), and chronic (ferritin and hemosiderin, short T2). The short T1 of methemoglobin is due to the paramagnetic dipole-dipole interaction. Another paramagnetic property, the magnetic susceptibility effect, is responsible for the short T2 observed when deoxyhemoglobin, methemoglobin, or hemosiderin is intracellular. T2 shortening can also be produced by hemoconcentration and clot retraction. The T2 shortening due to magnetic susceptibility effects is enhanced on higher-field-strength systems and on gradient-echo images and is reduced with "fast spin-echo" MR techniques.