Introduction

Under normal physiological conditions, neurons do not come in direct contact with blood. The blood–brain barrier, consisting of astrocyte end feet, extracellular matrix, and endothelial cells, forms an elaborate meshwork that surrounds blood vessels and regulates the selective passage of blood elements and nutrients to the neurons. When an artery in the brain ruptures, blood envelopes cells in the surrounding tissue, upsets the blood supply provided by the injured vessel and disturbs the delicate chemical equilibrium essential for neurons to function. This is called hemorrhagic stroke and accounts for approximately 20% of all strokes.

Hemorrhagic stroke has been less investigated than ischemic stroke although it represents a significant clinical problem. Direct tissue destruction, tissue compression around the hematoma, and an inflammatory response lead to neuronal injury and neurological deficits after hemorrhagic strokes. The size of the hematoma has a direct relationship with the clinical outcome. The hematoma causes mass effect and compresses the surrounding tissue, contributing to the neuronal death at the margin of the hematoma and in the penumbral region around the hematoma. Decreasing the space-occupying effect by aspiration of the hematoma and decreasing inflammation ameliorate the neurological deficits after hemorrhagic stroke.

A number of experimental cerebral hemorrhagic models have been developed to study the mechanisms underlying cerebral bleeding and resulting pathophysiology. The knowledge gained has helped in identifying many factors that contribute to rupture of an artery or an aneurysm.