Excerpt from Brain, Hypertensive Hemorrhage

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Background

Spontaneous intracranial hemorrhage affects 37,000 people in the United States each year, comprising 10-20% of stroke occurrences. In adults who present with nontraumatic intraparenchymal hemorrhage in the brain, hypertension is the most common etiology. Intracerebral hemorrhage (ICH) occurs when damaged arteries bleed directly into the brain substance.

For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.

Pathophysiology

Increased blood pressure damages the cerebral vessels primarily in two ways. Chronic hypertension stimulates the brain's blood vessels to make gradual, adaptive changes in an attempt to preserve the blood-brain barrier. One gradual change that may develop is lipohyalinosis. Subintimal fibroblast proliferation occurs, with an accumulation of lipid-laden macrophages and cholesterol deposits; this results in hyalinization and lipidosis of the blood vessels. This process segmentally affects the smaller penetrating arteries (<200 mm in diameter) and may account for many lacunar infarcts of the basal ganglia and thalamus, which seem to occur without known symptoms. Lipohyalinosis may be an intermediate stage between fibrinoid necrosis from severe hypertension and microatheromas from long-standing hypertension.

Plasma leakage from persistently elevated blood pressures also can result in hyaline degeneration of the cerebral blood vessels. Serum protein accumulates in the basement membranes of the arterioles and results in collagen formation. Arterial sclerosis and fibrinoid necrosis may occur, as well as focal aneurysmal dilatation (Charcot-Bouchard intracerebral microaneurysm).

Two theories about the mechanism of intracranial bleeding related to hypertensive small-vessel disease have been developed as follows:

• The first theory states that the hemorrhage may arise from rupture of the damaged blood vessel. The rupture is believed to occur at Charcot-Bouchard aneurysms. This theory remains controversial. Studies have reported incidences of hypertensive ICH that occurred in the absence of these microaneurysms. What are believed to be aneurysms actually may be the twists and coils of tortuous small vessels, which on cross section with some histologic stains may mimic the appearance of Charcot-Bouchard aneurysms.
• The second theory states that brain infarction eventually results in vascular compromise. The first theory, intraparenchymal hemorrhage secondary to rupture of the vessel, is accepted more widely.

Frequency

United States

Spontaneous ICH causes 10-20% of strokes and 15-20% of stroke-related deaths.

The overall incidence of ICH is estimated at 9 per 100,000. Of these patients, 70-90% suffer from high blood pressure.

International

Approximately 10-18% of deaths in Western Europe result from intracerebral hematomas.

The incidence and death rate in Japan is 4-6 times higher than in Western Europe and the United States. The higher rate in Japan may be related to diet, as a decrease in overall incidence of intracerebral hemorrhage has been associated with westernization of the Japanese diet after World War II.

Mortality/Morbidity

According to reports, stroke is the third most common cause of mortality in the United States and may be responsible for approximately 2-4% of deaths.

Spontaneous ICH causes 10-20% of strokes and 15-20% of stroke-related deaths.

Race

The incidence of spontaneous ICH may be higher among black persons than white persons, since a higher incidence of hypertension is seen in black persons younger than 45 years.

Sex

Men have a 5-20% higher incidence of ICH than women.

Age

Of spontaneous ICH patients, 90% are older than 45 years.

Anatomy

The arteries in the brain damaged by exposure to chronic hypertension typically are the perforator arteries, which serve the basal ganglia, thalamus, and pons. Other areas that also may be affected include the centrum semiovale and, occasionally, the cerebellum. The areas with arteriolar damage are prone to lacunar infarcts and hypertensive hemorrhages.

The areas in which hypertensive hemorrhages most commonly occur are the basal ganglia and thalamus (see Picture 1). Predominantly, hemorrhages of the basal ganglia involve the putamen and are fed by the lenticulostriate arteries. Complications of focal hemorrhages include edema, ischemia, and infarct. If the hemorrhage is large enough and in the appropriate location, it may result in noncommunicating or obstructive hydrocephalus by compressing the foramen of Monro, the third ventricle, or the aqueduct of Sylvius. In contrast, extension of a parenchymal bleed into the ventricles may result in communicating hydrocephalus.

Secondary intraventricular hemorrhage (IVH) may occur in one third to one half of patients with spontaneous ICH as a result of arterial hypertension and/or small arteriolar degeneration. IVH is seen most often with thalamic, putaminal, or caudate nucleus hemorrhages, which can extend medially a short distance directly into the lateral or third ventricles. IVH in these patients clearly has been associated with larger ICH, midline shift, and increased morbidity and mortality.

Hypertensive hemorrhages in the cerebellum (see Picture 2, Picture 3) tend to occur adjacent to the dentate nucleus or in the deep white matter, depending on the perforating branches of the superior cerebellar or posterior inferior cerebellar arteries. Expansion of the hematoma may result in rupture into the fourth ventricle or extension into the contralateral side. Less frequently, hypertensive bleeds may occur in the cerebral white matter.

Clinical Details

Compared to the chronic effects of hypertension, relatively sudden elevations in blood pressure may cause neurologic consequences via a different mechanism. An acute episode of severe hypertension can cause breakdown of the blood-brain barrier, resulting in increased vascular permeability and focal edema. This may occur especially at blood pressures greater than 220/140, because the brain is no longer protected by autoregulation above this pressure. This possibly contributes to hypertensive encephalopathy. The more vulnerable areas are primarily the regions supplied by the posterior circulation where less sympathetic control of autoregulation exists.

This situation may be aggravated by the thickened arteriolar walls of chronic hypertension, which do not allow normal vasoconstriction. In turn, this may cause cerebrovascular autoregulation to reset at higher pressures. Findings of capillary damage and vascular necrosis have been identified in situations of hypertensive encephalopathy and eclampsia. Thickened walls also increase vascular resistance. Consequently, collateral reserve is decreased, predisposing the brain to ischemic events.

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.

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