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tions In the rst hours and days following the hemorrhage, a limited amount of edema accumulates around the clot and adds to the mass effect Hydrocephalus may occur as a result of bleeding into the ventricular system or from compression of the third ventricle Extravasated blood undergoes a predictable series of changes At rst uid, it clots within hours Before the clot forms, red cells may settle in the dependent part of the hematoma and form a meniscus with the plasma above; this is particularly prone to occur in cases of anticoagulant-induced hemorrhage A uid- uid level is then observed on scans ( hematocrit effect ) Only masses of red blood cells (RBCs) and proteins are found within the hematoma; rarely one sees a few remnants of destroyed brain tissue The hematoma is surrounded by petechial hemorrhages from torn arterioles and venules Within a few days, hemoglobin products, mainly hemosiderin and hematoidin, begin to appear The hemosiderin forms within histiocytes that have phagocytized RBCs and takes the form of ferritin granules, which stain positively for iron As oxyhemoglobin is liberated from the RBCs and becomes deoxygenated, methemoglobin is formed This begins within a few days and imparts a brownish hue to the periphery of the clot Phagocytosis of RBCs begins within 24 h, and hemosiderin is rst observed around the margins of the clot in 5 to 6 days The clot changes color gradually, over a few weeks, from dark red to pale red, and the border of golden-brown hemosiderin widens The edema disappears over many days or weeks In 2 to 3 months, larger clots are lled with a chrome-colored mush, which is slowly absorbed, leaving a smooth-walled cavity (slit hemorrhage) or a yellow-brown scar The iron pigment (hematin) becomes dispersed and studs adjacent astrocytes and neurons It may persist well beyond the border of the hemorrhage for years In CT scans, fresh blood is visualized as a white mass as soon as it is shed The mass effect and the surrounding extruded serum and edema are hypodense After 2 to 3 weeks, the surrounding edema begins to recede and the density of the hematoma decreases, rst at the periphery Gradually the clot becomes isodense with brain There may be a ring of enhancement from the hemosiderin lled macrophages and the reacting cells forming the capsule of the hemorrhage By MRI, either in conventional T1- or T2weighted images, the hemorrhage is not easily visible in the 2 or 3 days after bleeding, since oxyhemoglobin is diamagnetic or, at most, is slightly hypointense, so that only the mass effect is evident After several days the surrounding edema is hyperintense in T2weighted images As deoxyhemoglobin and methemoglobin form, the hematoma signal becomes bright on T1-weighted images and dark on T2 As the hematoma becomes subacute, the dark images gradually brighten When methemoglobin disappears and only hemosiderin remains, the entire remaining mass is hypodense on T2weighted images, as are the surrounding deposits of iron MR images that display areas of magnetic susceptibility will show hemorrhages earlier and detect remnants of deposited hemosiderin even years afterwards Hemorrhages may be described as massive, moderate, small, slit, and petechial Massive refers to hemorrhages several centimeters in diameter; small applies to those 1 to 2 cm in diameter and less than 20 mL in volume; a moderate-sized hemorrhage, of course, falls between these two, both in diameter and in volume Slit refers to an old collapsed hypertensive or traumatic hemorrhage that lies just beneath the cortex Pathogenesis The hypertensive vascular lesion that leads to arterial rupture in some cases appears to arise from an arterial wall.

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altered by the effects of hypertension, ie, the change referred to in a preceding section as segmental lipohyalinosis and the false aneurysm (microaneurysm) of Charcot-Bouchard Ross Russell has af rmed 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 our colleague C M Fisher, 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 represent sites of secondary rupture from tearing of small vessels by the expanding hematoma Clinical Picture Of all the cerebrovascular diseases, brain hemorrhage is the most dramatic and from ancient times has been surrounded by an aura of mystery and inevitability It has been given its own name, apoplexy The prototype is an obese, plethoric, hypertensive male who, while sane and sound, 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 pro le of a stroke, ie, an abrupt onset of symptoms that evolve gradually and steadily over minutes or hours, depending on the size of the ruptured artery and the speed of bleeding Several general features of intracerebral hemorrhage should be emphasized Acute reactive hypertension, far exceeding the patient s chronic hypertensive level, is a feature that should always suggest hemorrhage; it is seen with moderate and large clots situated in deep regions Vomiting at the onset of intracerebral hemorrhage occurs much more frequently than with infarction and should always suggest bleeding as the cause of an acute hemiparesis Severe headache is generally considered to be an accompaniment of intracerebral hemorrhage and in many cases it is, but in almost 50 percent of our cases headache has been absent or mild in degree Nuchal rigidity is found frequently; but again, it is so often absent or mild that failure to nd it should does not eliminate the diagnosis (Stiffness of the neck characteristically disappears as coma deepens) It should also be noted that the patient is often alert and responding accurately when rst seen This can be true even when the CSF is grossly bloody; thus the adage that hemorrhage into the ventricular system always precipitates coma is quite incorrect Only if bleeding into the ventricles is massive will coma result Seizures, usually focal, occur in the rst few days in some 10 percent of cases of supratentorial hemorrhage, rarely at the time of the ictus but more commonly as a delayed event, months or even years after the hemorrhage, in association with subcortical slit hemorrhages The fundi often show hypertensive changes in the arterioles Rarely, white-centered retinal hemorrhages (Roth spots) or fresh preretinal (subhyaloid) hemorrhages occur; the latter are much more common with ruptured aneurysm, arteriovenous malformation, or severe trauma Headache, acute hypertension, and vomiting with a focal neurologic de cit are therefore the cardinal features and serve most dependably to distinguish hemorrhage from ischemic stroke Very small hemorrhages in silent regions of the brain may escape clinical detection Hemorrhages that complicate the administration of anticoagulants, like those from some vascular malformations, may evolve at a slower pace Usually there are no warn-.

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