Spontaneous intracerebral hemorrhages

Dernière mise à jour : Friday 20 February 2015

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Spontaneous intracerebral (intraparenchymal) hemorrhages (SICH) are characterized by a non-traumatic bleeding into the brain parenchyma.
They account for 10 to 15% of cerebrovascular accidents (CVA) (stroke), and together with subarachnoid hemorrhage, are categorized as hemorrhagic strokes.
They are primary in most cases, that is, in relation to the rupture of small vessels damaged by high blood pressure (hypertension) or chronic amyloid angiopathy (11). They can also be secondary (20% of the cases) to an underlying macroscopic lesion such as an arterial aneurysm, an arteriovenous malformation, a tumor or related to any cause of coagulopathy. Only primary ICH will be covered in this chapter.

 1 - Epidemiology

The annual incidence of primary ICH is between 10 to 20 cases per 100,000 inhabitants. It increases with age (2/3 occur after the age of 75), and is higher among males (12,15,41). Contrary to what is observed for cerebral infarctions, the overall incidence of ICH has not declined in the past decades (45). Epidemiological studies suggest a decrease in the incidence of ICH in patients under 75 years (probably due to a better management of hypertension) and an increase in the elderly (due to amyloid angiopathy and antithrombotic drugs). Finally, the risk of ICHs is increased in the Asian population (45).

 2 - Risk Factors (RF)

Known risk factors for primary SICH include (1):

  • a- HBP: This is the single most important RF, especially in smokers (5). The risk correlates with the severity of hypertension. A good blood pressure control can decrease this risk (21).
  • b- Alcohol consumption increases the risk of primary SICH by inducing changes in brain vasculature and disrupting hemostasis (25).
  • c- Other RFs are more anecdotal and include: diabetes mellitus, factor ΧIII mutation, the presence of ε2 and ε4 alleles of the apolopoprotein E gene (1,7,34).

 3 - Anatomopathology

 a- Causal lesions

Two types of lesions account for the rupture of small cerebral vessels and are both secondary to chronic hypertension: hypertensive angiopathy and amyloid angiopathy.

  • Hypertensive angiopathy: chronic hypertension induces a reduction in arterial compliance. These vessels which are more rigid, will therefore have a decreased tolerance to potential spurts in blood pressure, thus a tendency to rupture. This phenomenon is observed mainly in small perforating arteries (50-700 μm in diameter) as reflected in the topographic distribution of the hematoma (see Anatomy) (42). There are often several sites of rupture, characterized by a breach in the elastic layer, atrophy of smooth muscle and cellular degeneration. This is often associated with atherosclerotic lesions. Historically in 1868, Charcot and Bouchard attributed the vascular rupture to the presence of micro aneurysms (called Charcot-Bouchard microaneurysms). However, electron microscopic studies have actually shown that these lesions are sub-adventitial hemorrhages, outdating the concept of microaneurysms (10,42).
  • Amyloid angiopathy: it is characterized by the presence of β-amyloid deposits in small and medium size arteries, thus inducing degenerative lesions of the arterial wall. These lesions are mainly located in the cortical leptomeningeal arteries and the cerebellum, hence explaining the topographic predilection of the hematoma at these sites.

 b-The hematoma

The blood usually clots within the cleavage planes of the white matter, with a relatively limited neuronal destruction. However, under the influence of different toxins released in-situ, peri-lesional edema, neuronal damage and infiltration by macrophages and neutrophils occurs (32).