AUTHOR AND EDITOR INFORMATION

Section 1 of 7  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Multimedia
• References

INTRODUCTION

Section 2 of 7  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Multimedia
• References

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.

DIFFERENTIALS

Section 3 of 7  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Multimedia
• References

Other Problems to be Considered

Underlying brain lesions (ie, tumor, vascular malformation)
Ruptured aneurysm

CT SCAN

Section 4 of 7  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Multimedia
• References

Findings

Once an ICH occurs, the most efficient way to localize the hemorrhage is by CT. 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.

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 findings over time are as follows:

• 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.

MRI

Section 5 of 7  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Multimedia
• References

Findings

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.

Recent 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 (see Picture 4, Picture 5).

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.

Please refer to Brain, MRI Appearance of Hemorrhage for more details.

MULTIMEDIA

Section 6 of 7  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Multimedia
• References

Media file 1:  A 59-year-old female with hypertension who presented with left-sided weakness demonstrated a right putaminal hemorrhage on noncontrast CT examination of the head. Tiny hyperdense foci in the basal ganglia and pineal gland represent calcifications.
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Media type:  CT

Media file 2:  A 62-year-old female with hypertension presented with acute-onset ataxia and confusion. Noncontrast CT examination of the head showed a large right cerebellar hemorrhage, which was evacuated to relieve the mass effect on the brainstem and fourth ventricle.
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Media type:  CT

Media file 3:  Cerebellar hemorrhage of a 62-year-old female with hypertension seen on T2-weighted MRI (same patient as Picture 2)
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Media type:  MRI

Media file 4:  T2-weighted MRI through the thalami of a hypertensive patient demonstrates two small areas of decreased signal in the right thalamus, representing hemorrhagic lacunes.
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Media type:  MRI

Media file 5:  T2-weighted gradient-echo MRI through the thalami demonstrates multiple, bilateral foci of signal loss, correlating with expected locations of hypertensive petechial hemorrhages that were not seen on regular T2-weighted images (same patient as Picture 4).
	View Full Size Image
Media type:  MRI

REFERENCES

Section 7 of 7

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Multimedia
• References

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• Fazekas F, Kleinert R, Roob G. Histopathologic analysis of foci of signal loss on gradient-echo T2*- weighted MR images in patients with spontaneous intracerebral hemorrhage: evidence of microangiopathy-related microbleeds. AJNR Am J Neuroradiol. Apr 1999;20(4):637-42. [Medline].
• Gokaslan ZL, Narayan RK. Intracranial Hemorrhage in the Hypertensive Patient. Neuroimaging Clinics of North America. 1992;2:171-86.
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• Nelson JS, Parisi JE, Schochet SS Jr. Principles and Practise of Neuropathology. Mosby - Year Book, Inc. St. Louis, MO;1993.
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• Ruscalleda J, Peiro A. Prognostic factors in intraparenchymatous hematoma with ventricular hemorrhage. Neuroradiology. 1986;28(1):34-7. [Medline].
• Spangler KM, Challa VR, Moody DM. Arteriolar tortuosity of the white matter in aging and hypertension. A microradiographic study. J Neuropathol Exp Neurol. Jan 1994;53(1):22-6. [Medline].
• Taveras JM, Pile-Spellman J. Neuroradiology. 3rd ed. Williams & Wilkins;1996.
• Welch KMA, Caplan LR, Reis DJ, Weir B, Siesjo BK, eds. Primer on Cerebrovascular Diseases. Morgan Kaufmann;1997.

Article Last Updated: Oct 26, 2004