Spontaneous Intracerebral Hematoma

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Etiology

The majority of intracerebral hemorrhages are associated with hypertension, which affects the small parenchymal arteries and arterioles and leads to fibrosis, hyalinosis, and fibrinoid necrosis. Such diseased arteri-oles easily rupture, causing the hemorrhage.

Less common causes of hemorrhages are vascular malformations, vasculopathies, hemorrhagic diseases, and hemorrhage within tumors (see Table 4.10; also see the section, Various Stroke Etiologies).

Pathology

Hypertensive hemorrhages have predilections for the basal ganglia (50%), the thalamus (10%), the pons and the cerebellum (5%-15%). Less common sites are the cerebral hemispheric white matter (lobar hemorrhage) and the ventricles (Fig. 4.24). Large basal ganglia and thalamus hemorrhages are accompanied by significant edema and may, during the first days, extend into the ventricles. A variant of basal ganglia hemorrhage occurs in the head of the caudate nucleus, which is supplied by the lateral striatal arteries. The pontine hemorrhage

FIGURE 4.23

Vascular images. A. MRA of a 69-year-old man with history of TIAs in the vertebrobasilar circulation shows occlusion of the left vertebral artery and stenosis of the basilar artery. B. CT scan of a 62-year-old man shows a recent large left-MCA infarct. C. Color-flow Doppler shows sharp occlusion of the left ICA and severe stenosis of the right ICA. D. Conventional angiogram in a 70-year-old man with history of TIAs in carotid circulation shows severe stenosis of ICA above the bifurcation.

TABLE 4.10.

Cerebral Hemorrhage

Cerebral Hemorrhage

Hypertension

Cerebral Hemorrhage

Subarachnoid

Vascular malformation

Amyloid angiopathy Vasculopathy/Vasculitis Hemorrhagic diseases Iatrogenic complications

Subarachnoid

Arteriolosclerosis

Vascular malformation

Amyloid angiopathy Vasculopathy/Vasculitis Hemorrhagic diseases Iatrogenic complications

Rupture of berry aneurysm may occupy the basis or may form confluent hemorrhages in the tegmentum and the basis. A large cerebel-lar hemorrhage carries the risk of tonsillar herniation, subsequent medullary compression, and acute respiratory failure. Early diagnosis and surgical evacuation of the clot is life saving.

The hematoma breaks down and liquefies after a few days. Its resorption may take several weeks or even months, depending on the size. Ultimately, a cystic cavity, with brown-stained walls from hemosiderin, replaces the hematoma (see Fig. 4.24).

Hematoma Intracerebral

FIGURE 4.24

Topographic distribution of hypertensive intracerebral hemorrhages. A. Small putaminal hemorrhage. B. Massive basal ganglia hemorrhage extending into the ventricle. The parenchyma surrounding the hemorrhage is swollen, and the ventricle is compressed. C. Massive basal ganglia hemorrhage ruptured into the ventricle. D. Small caudate hemorrhage associated with massive ventricular hemorrhage. E. Thalamus hemorrhage. F. Pontine hemorrhage. G. Cerebellar hemorrhage. Note the herniation of the cerebellar tonsils. H. Cystic cavities with brown stained walls from hemosiderin at the site of resolved basal ganglia hemorrhage.

FIGURE 4.24

Topographic distribution of hypertensive intracerebral hemorrhages. A. Small putaminal hemorrhage. B. Massive basal ganglia hemorrhage extending into the ventricle. The parenchyma surrounding the hemorrhage is swollen, and the ventricle is compressed. C. Massive basal ganglia hemorrhage ruptured into the ventricle. D. Small caudate hemorrhage associated with massive ventricular hemorrhage. E. Thalamus hemorrhage. F. Pontine hemorrhage. G. Cerebellar hemorrhage. Note the herniation of the cerebellar tonsils. H. Cystic cavities with brown stained walls from hemosiderin at the site of resolved basal ganglia hemorrhage.

FIGURE 4.25

CT images of hypertensive cerebral hemorrhages. A. Nonenhanced axial CT scans show an acute hyperdense hemorrhage extending into the ventricle. B. Acute hyper-dense lobar hemorrhage in the frontal lobe extends into the anterior horn.

Clinical Features

Hypertensive intracerebral hemorrhage accounts for about 10% to 12% of all strokes. The onset is abrupt. Generalized symptoms include headaches, vomiting, confusion, depressed consciousness ranging from stupor to coma and, in some patients, seizures. Focal symptoms indicate the site of the hemorrhage. Expansion of the hemorrhage and edema may continue, causing deterioration for about 24 hours. Early mortality remains high, at 30% to 40%.

CT scan readily demonstrates the acute parenchy-mal hematoma as a hyperdense (bright) lesion, usually surrounded by a hypodense area caused by edema (Fig. 4.25). Acute hemorrhage on MR T1-weighted images appears as a hypointense (dark) and on T2-weighted images as a hyperintense (bright) lesion. With time, as the oxyhemoglobin gradually disintegrates into methemoglobin and then into hemosiderin, the appearance of the hemorrhage changes. An old hemorrhage on the CT scan appears as a hypodense lesion indistinguishable from an old infarct and, on T1- and T2-weighted MR images, as a hypointense lesion (see Table 4.9).

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