Introduction

Nontraumatic intracerebral hemorrhage (ICH) accounts for approximately 10% to 15% of all cases of stroke and is associated with high rates of morbidity and mortality (1-5). To date, no proven specific or effective treatment for ICH exists, nor do clear guidelines regarding management of blood pressure and appropriate timing and indications for performing surgery (6). One of the limitations in developing interventional protocols is the fact that we lack knowledge regarding the temporal response of the human brain to ICH because we have no good test to measure it and much of what we know is based on the animal model. A better understanding of the pathophysiology of the perilesion injury is required in order to develop new therapeutic strategies.

We know that, initially, the hemorrhage spreads between planes of white matter, with minimal destruction, leaving nests of intact neural tissue within and surrounding the hematoma (7,8). However, later, the hematoma is known to potentially expand, mainly in the first 24 hr, and cause additional neuronal damage (9,10). In addition to the mass effect observed in the beginning, the presence of a hematoma induces 3 early pathophysiologic changes in the surrounding parenchyma: neuronal and glial cell death, vasogenic edema, and breakdown of the blood-brain barrier (BBB), accounting for more expansion and cell death (11). It is theorized that tissue damage from ICH is related to both the presence of a mass and to mediators that exist in blood, supported by the observations that hematomas of the same size cause different outcomes in different individuals and that no edema was formed in an animal model when a microballoon was inserted in the caudate nucleus, despite increased intracranial pressure and decreased cerebral blood flow (CBF) (12).

In the past (13-15), ischemia from mass effect was thought to be the main process of neuronal injury and edema following ICH. However, it is now accepted that blood and plasma products play a more important role in secondary brain injury after ICH (16-19). Other mediators considered to cause additional brain damage following ICH are excitatory amino acids, matrix metalloproteinases (MMPs), and mediators of inflammation. This chapter reviews current understanding of brain injury mechanisms following ICH in an effort to further the investigation for development of effective therapies for the future.

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