A stroke is considered truly hemorrhagic if blood is found within the first 24 hours after initial symptoms. When blood is noted after this time, it is usually hemorrhagic transformation of an ischemic stroke, which is due to reperfusion injury.
Hypertension is the most common cause of intraparenchymal hemorrhage, which can also be caused by ruptured aneurysm, arteriovenous malformation, and more rarely, by infarction, neoplasms, blood coagulation defects, and cerebral arteritis (81). Common hemorrhage sites include the putamen and the thalamus, which receive their major blood supply from the lenticulostriate and the thalamogeniculate arteries, respectively.
Because freshly extravasated blood is more radiodense than gray or white matter, an acute hemorrhagic stroke is well visualized by CT as a hyperdense region usually conforming to an arterial distribution (Fig. 6-84A,B). The radiodensity of the blood clot increases over 3 days because of clot retraction, serum extrusion, and hemoglobin concentration. The extruded serum may form a hypodense rim around the hyper- dense clot (Fig. 6-84C). As edema develops over 3 to 5 days, the hypodense rim may increase. Eventually, the hyperdensity of the clot gradually fades and usually disappears by 2 months, leaving only a narrow hypodense slit to mark the site where hemorrhage took place (Fig. 6-84D).
FIGURE 6-84. CT evaluation of early and evolving hemorrhagic strokes. A: Recent hemorrhagic stroke has occurred in the distribution of the right posterior cerebral artery, which appears hyperdense (arrows). B: A massive hypertensive hemorrhage involving most of the interior of the left cerebral hemisphere with intraventricular hemorrhage, midline shift to the right, and herniation of the left hemisphere under the falx cerebri. C: A 5-day-old hemorrhagic stroke involving the lenticular nucleus shows a hyperdense hemorrhagic center (arrow ) and a hypodense edematous rim (arrowhead). D: The same stroke patient displays replacement of the hyperdense hemorrhage with a narrow hypodense interval (arrows) several months later.
The appearance of hemorrhage by MRI depends on the state of the hemoglobin in the hemorrhage (81). The oxyhemoglobin present in a fresh hemorrhage is nonparamagnetic; therefore, very early hemorrhage is not detected by MRI. Within a few hours, the oxyhemoglobin will be converted to deoxyhemoglobin, which is a paramagnetic substance. Intracellular deoxyhemoglobin will cause acute hemorrhage to appear very hypointense on T2-weighted images and slightly hypointense or isointense on T1-weighted images (Fig. 6-85A). By 3 to 7 days, intracellular deoxyhemoglobin is oxidized to methemoglobin as the clot enters the subacute phase. Although a subacute hemorrhage has several subphases in which the signal intensity of methemoglobin varies, in general methemoglobin appears hyperintense on both T1- and T2-weighted images (Fig. 6-85B). Because the conversion to methemoglobin begins at the periphery of the clot, early in the subacute phase a hemorrhage can have a hyperintense margin and a central hypointense region still containing deoxyhemoglobin. Eventually the entire region of subacute hemorrhage becomes hyperintense. Over several months, the methemoglobin is gradually resorbed and the clot develops a rim of hemosiderin- containing macrophages. Hemosiderin is hypointense on both T1- and T2-weighted images. Therefore, a chronic hemorrhage of several months duration often has a hyperintense methemoglobin center and a hypointense hemosiderin rim. Because the hemosiderin deposits remain indefinitely, an old hemorrhage of several years duration shows up as a totally hypointense area. Gradient-echo sequences have recently been added to many brain MRI protocols, as they are very sensitive in the detection of degrading blood products, which appear as areas of hypointensity. As can be seen, CT provides the very earliest information about cerebral hemorrhage, whereas MRI is the better technique for determining hemorrhage age.