Brain Imaging in Hypertensive Hemorrhage 

Spontaneous intracranial hemorrhage affects approximately 40,000 people in the United States each year, comprising 10-20% of stroke occurrences.^[1] In adults who present with nontraumatic intraparenchymal hemorrhage in the brain, hypertension is the most common etiology.^{[2, 3, 4]} Intracerebral hemorrhage (ICH) occurs when damaged arteries bleed directly into the brain substance. (See the images below.)

Preferred examination

CT is efficient and sensitive in detecting ICH. This test may be followed by MRI to evaluate for possible underlying lesions and to gain more detailed information about a hemorrhage.^[5]

Once an intracerebral hemorrhage (ICH) occurs, the most efficient way to localize the hemorrhage is by CT (see images below). The appearance of a bleed on CT depends on the elapsed time since the event. If imaged in the acute stage (within approximately 4 h), the hemorrhage is seen as an area of increased attenuation, measuring from 40-90 Hounsfield units. The high attenuation of an acute intracranial bleed on CT may persist for approximately 1 week. The increased density of blood in relation to the surrounding parenchyma of the brain relates to the hemoglobin protein contained in extravasated blood. Therefore, in severely anemic patients, look carefully for acute blood that may be isodense or hypodense to the brain.^{[5, 6]}

A surrounding area of low attenuation may be seen surrounding the blood, representing brain edema or extruded serum. Blood seen in the hyperacute stage may demonstrate a fluid-fluid level, representing the sedimentation of blood that has extravasated but has not clotted yet. A fluid-fluid level also may be seen in patients who have bled into a preexisting cyst or cavity or in patients who have received anticoagulants.

As the hemorrhage evolves, different characteristic appearances can be identified on CT, depending on the age of the bleed.

CT scan findings over time

After 7-10 days, the high density of blood begins to decrease starting from the periphery of the lesion.

From 1-6 weeks, peripheral enhancement can be seen. It mimics the appearance of an abscess, possibly related to hypervascularity at the periphery of a resolving hematoma or disruption of the blood-brain barrier.

By 2-4 months, decreased density indicates cavity formation. A residual cavity is the final stage, which is reached after complete absorption of necrotic and hemorrhagic tissue.

On MRI, the stage of a hemorrhage can be delineated based on the chemical changes that occur in the hemoglobin molecule as the hemorrhage evolves. T1 and T2 imaging sequences also can be used.^{[5, 7, 8, 9, 10]}

Studies have described patterns of scattered, multifocal, hypointense lesions or areas of signal loss on T2-weighted gradient-echo MRI, in a distribution that correlates with areas of petechial hemorrhages in the autopsied brains of patients with chronic hypertension, as shown in the images below.

These lesions were seen in the basal ganglia and thalamus, as well as in the centrum semiovale and cerebellum. These lesions seen on MRI may represent hemosiderin deposits from petechial hemorrhages related to hypertension, although histopathologic-correlative studies have not proven this consistently. Nevertheless, these foci of abnormal MRI signal hypointensity overlap with areas of small-vessel disease attributed to chronic hypertension.