1. There is a constant sequence of signal intensity patterns that characterize 1.5 T, spin echo MR images of hemorrhagic lesions. 2. The MRI appearance of intraparenchymal hemorrhage is determined by the sequential chemical degradation of Hb, by the paramagnetic properties of the degradation products and by certain biologic factors including pO2, edema formation, hematocrit and BBB. 3. Acute intraparenchymal hemorrhage is characterized by markedly diminished signal intensity centrally relative to surrounding white matter (hypointensity) on T2 weighted images and often by a moderately increased signal intensity (hyperintensity) of the adjacent white matter produced by surrounding edema on proton density and T2 weighted images. 4. Early subacute intraparenchymal hemorrhage is characterized centrally by moderate hypointensity on T2 weighted images, and peripherally, by moderate hyperintensity on T1 weighted and marked hypointensity on T2 weighted images. Hyperintensity on proton density and T2 weighted images of nearby white matter owing to edema may again be seen. 5. Late subacute intraparenchymal hemorrhage is characterized by marked peripheral and central hyperintensity on both T1 and T2 weighted images. Also, marked hypointensity of the adjacent brain rim on T2 weighted images owing to hemosiderin deposition may be seen. 6. Chronic intraparenchymal hemorrhage is characterized by marked hyperintensity both centrally and peripherally on both T1 and T2 weighted images and by marked hypointensity of the adjacent brain rim on T2 weighted images owing to hemosiderin deposition. Surrounding edema is no longer present. 7. The integrity of the blood-brain barrier appears to be important in determining whether or not hemosiderin accumulations consistently occur in subacute and chronic hemorrhage. 8. Hemorrhagic conditions in which the defined sequence of signal intensity patterns may be seen include: venous thrombosis, hemorrhagic infarction, occult vascular malformation and intracranial aneurysm.