Imaging techniques demonstrate a predictable sequence of changes as shown in Fig. 33-24. On CT, fresh blood is visualized as a white mass as soon as it is shed. The “spot sign,” the appearance of contrast within the hemorrhage during CT angiography, is associated with a high rate of hematoma expansion. The mass effect and the surrounding extruded serum and edema are hypodense on CT. After 2 to 3 weeks, the surrounding edema begins to recede and the density of the hematoma decreases, first at the periphery. Gradually the clot becomes isodense with brain. There may be a ring of enhancement from the hemosiderin-filled macrophages and the reacting cells that form a capsule for the hemorrhage. At one point several weeks after the bleed, the appearance may transiently simulate a tumor or abscess. By MRI, either in conventional T1or T2-weighted images, the hemorrhage is not easily visible in the 2 or 3 days after bleeding, as oxyhemoglobin is diamagnetic or, at most, is slightly hypointense, so that only the mass effect is evident. MR gradient echo or equivalent sequences that display areas of magnetic susceptibility show hemorrhages earlier and detect remnants of deposited hemosiderin even years afterward.
After several days the surrounding edema is hyperintense in T2-weighted images. As deoxyhemoglobin and methemoglobin form, the hematoma signal becomes bright on T1-weighted images and dark on T2. The hematoma is then subacute and the dark signal gradually brightens. When methemoglobin disappears and only hemosiderin remains, the entire remaining mass is hypodense on T2-weighted images, as are the surrounding deposits of iron. The sizes of cerebral hemorrhages vary widely. Massive refers to hemorrhages several centimeters in diameter, usually larger than 50 mL; small applies to those 1 to 2 cm in diameter and less than 20 mL in volume. The volume and location relate to outcome and the nature of the initial neurologic deficit.
The hypertensive vascular lesion that leads to arteriolar rupture in most cases appears to arise from an arterial wall altered by the effects of hypertension, that is, the change referred to in a preceding section as segmental lipohyalinosis and the false aneurysm (microaneurysm) named for Charcot and Bouchard. Ross Russell’s work affirmed the relationship of these microaneurysms to hypertension and hypertensive hemorrhage and their frequent localization on penetrating small arteries and arterioles of the basal ganglia, thalamus, pons, and subcortical white matter. However, in the few hemorrhages examined in serial sections by C.M. Fisher (1959), the bleeding could not be traced to Charcot-Bouchard aneurysms. Takebayashi and coworkers, in an electron microscopic study, found breaks in the elastic lamina at multiple sites, almost always at bifurcations of the small vessels. Possibly these represented points of secondary rupture from tearing of small vessels by the expanding hematoma. Amyloid impregnation of vessel walls represents a different mechanism for vessel rupture, as discussed further on.
Of all the cerebrovascular diseases, brain hemorrhage is the most dramatic and from ancient times has been given its own name, “apoplexy.” The prototype was an obese, plethoric, hypertensive male who falls senseless to the ground—impervious to shouts, shaking, and pinching—breathes stertorously, and dies in a few hours. A massive blood clot escapes from the brain as it is removed postmortem. With smaller hemorrhages, the clinical picture conforms more closely to the usual temporal profile of a stroke, that is, an abrupt onset of symptoms that evolve gradually and steadily over minutes or hours, depending on the speed and expansion of bleeding.