Cerebral intraparenchymal hematoma (IH) is one of the most common causes of sudden onset of focal neurologic deficit. This is particularly true in the acute phase, in which IH appears hyperdense compared to the cerebral tissue. By three to four weeks, it becomes isodense with the cerebral gray matter and hypodense within 2 to 6 months. After contrast media administration, IH shows a peripheral ring of enhancement owing to the breakdown of the blood brain barrier. On magnetic resonance imaging (MRI), the appearance of IH depends upon the paramagnetic effects of the different derivates of hemoglobin and both the magnetic field strength and type of sequences used. In the hyperacute phase, IH appears hyperintense on T2 and hypointense on T1 owing to the presence of oxyhemoglobin. In the acute phase, IH is hypointense on T2 and iso-hypointense on T1 as a consequence of the presence of deoxyhemoglobin, which is converted into methemoglobin by 3 to 5 days. Methemoglobin has a strong paramagnetic effect, so in this phase IH becomes hyperintense on T1 and hypointense on T2. After 2 weeks, methemoglobin is converted in hemosiderin, responsible of the ring of hypointensity surrounding the lesion on T2WI. When an IH has been diagnosed, someone should think about the origin of bleeding. Among the different differential diagnosis, one should think about the possible origin, taking into account some parameters, such as: anamnestic data, site of the lesion, number of lesions, appearance on CT and MRI, and presence of perilesional edema. Computed tomography is a reliable and very fast tool for the diagnosis of IH, but MRI is able to provide additional information about the spontaneous or secondary nature of the hematoma, thus allowing a better characterization of the hemorrhagic lesion.