IV. INTRACEREBRAL HEMORRHAGE (hypertensive)

A. General Comments

Intracerebral hemorrhage accounts for about 15% of "strokes". It is much less common than infarction but more lethal - hemorrhage is the most common cause of death among cerebrovascular disorders. Intracerebral hemorrhage is most often due to hypertension, although there are a number of other etiologies, including AV malformation, ruptured aneurysm, and leukemia and associated blood dyscrasias. In this module, only hypertensive hemorrhage will be discussed.

B. Pathogenesis

Hypertension is associated with arteriolosclerosis (a disorder of small arteries and arterioles). Pathological changes in vessels include thickening of the vessel walls with increased cellularity, hyalinization of the media, and the formation of small (micro-) aneurysms known as Charcot-Bouchard aneurysms. Autoregulation is impaired and vascular permeability increases. Rupture of blood vessels results in hemorrhage into the substance of the brain, but the cause of rupture is not clear.

The thickened hyalinized wall of arterioles, as shown, is characteristic for arteriolosclerosis associated with hypertension.

C. Incidence

The age at onset is usually greater than 50. In most cases, occurrence is associated with chronic hypertension.

D. Most Common Sites

In the majority of cases hypertensive hemorrhage occurs in the area of the basal ganglia or thalamus. The pons and cerebellum are less common sites.

E. Clinical Course and Prognosis

In the majority of cases there is acute onset of headache and rapid development of stupor followed by coma. Signs and symptoms depend on the location of the hematoma. CT scan readily reveals the presence of an intracerebral hematoma. Hemorrhage is not instantly fatal - death occurs in 6-36 hours in 50-70% of patients. Patients who recover may have good return of neurologic functioning.

F. CSF Changes

CSF is often bloody because the hemorrhage may rupture directly into the subarachnoid space or intraventricular blood may enter the subarachnoid space via fourth ventricular outlet foramina.

G. Pathological Changes

The hemorrhage produces a large cavity filled with clot. This is a highly destructive, space-occupying lesion. Uncal herniation may occur with brainstem compression and secondary (Duret) brainstem hemorrhages. In cases of less severe hemorrhage, resolution may be associated with marked clinical improvement.

An intracerebral hemorrhage is present, extending into the ventricle.

The hemorrhage shown above caused increased intracranial pressure, leading to Duret hemorrages. The Duret (secondary) hemorrhages ( center of section) are shown in a brainstem section with midbrain structures at the top (aqueduct and colliculi), midbrain structures at the bottom right (cerebral peduncle and substantia nigra), pons structures at the bottom left (crossing fibers in pontine tegmentum).

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