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2Brain

hemorrhage often manifests as dizziness, vomiting, truncal ataxia, and gaze palsies.

Noncontrast CT is the most appropri-ate initial imaging study in patients with clinical stroke symptoms. If a parenchymal hemorrhage is the cause, the size of the bleed as well as any ventricular extension or secondary hydrocephalus are easily as-sessed. Acute hemorrhage (within four hours) appears as a well-defined area of high attenuation and may persist for up to a week. As the bleed ages, the margins be-come less distinct and a surrounding low-attenuation rim develops, reflecting brain edema or extruded serum. Subacute hema-tomas may show peripheral enhancement on postcontrast CT or MRI. Very remote hematomas appear as slitlike, CSF-density lesions.

The volume of a parenchymal hematoma(mL) is estimated by multiplying the threedimensions (in cm) and dividing the prod-uct by 2. Hematoma volumes > 50 mL areassociated with a poor prognosis (Fig. 2.17).

◆Hypertensive Hemorrhage

Twice as common as subarachnoid hem-orrhage, spontaneous intracranial hemor-rhage (ICH) comprises 10–20% of strokes, which are clinically indistinguishable from ischemic stroke and subarachnoid hemor-rhage. Patients with ICH often present with headache, nausea, and vomiting before a focal neurologic deficit becomes evident. In adults with nontraumatic intracranial hemorrhage, hypertension is the most common etiology.

In long-standing, poorly controlled hy-pertension, microaneurysmsdevelop in the perforating arterioles, primarily in the lenticulostriate, pontine, and cerebellar distributions. Accelerated atherosclero-sis and hyalinearteriosclerosis also play a part in the pathologic changes predispos-ing to hypertensive ICH. Bleeding usually occurs in the putamen, thalamus, pons, or cerebellum (in order of decreasing fre-quency), and clinical signs correspond to the location of hemorrhage and function of the involved brain. For example, cerebellar

Fig. 2.17a–fa,b Small hemorrhages in two patients. (a) Small focal hemorrhage in the right internal capsule genu and anterior thalamus. (b) Small left thalamic hemorrhage.

c,d Large left external capsule hemorrhage. Large left-sided hematoma with subfalcine shift, modest intraventricular hemorrhage, and trapping of the right lateral ventricle.

e,f Massive hemorrhage with rupture into the ventricular system and severe hydrocephalus. A large pa-renchymal hematoma obliterates the right basal ganglia and extends into the ventricles. Clot lls the third and fourth ventricles and causes marked hydrocephalus.