Abstract
Intracranial aneurysm rupture causes arterial bleeding into the subarachnoid space (SAH). In the acute stage lasting around 5 minutes intracranial pressure (ICP) rises rapidly up to the level between systolic and diastolic blood pressures, which slows down the outflow of blood, facilitates clot formation in the site of rupture and leads to arrest of bleeding. Increased ICP lowers cerebral perfusion pressure, causing brain ischemia, which is unevenly distributed throughout the brain as a result of interhemispheric pressure gradients, arterial spasms and other factors. No-reflow phenomenon in the capillaries following temporary arrest or considerable slowing of circulation produces areas of hypoperfusion and reduced capacity of blood flow autoregulation scattered irregularly in the brain in the subacute stage up to 30 minutes following haemorrhage. Disturbed regional cerebral blood flow is accompanied by spots of damaged blood brain barrier resulting in brain oedema. After SAH the brain remains vulnerable to reduction of blood flow and hypoxaemia, which explains greater brain damage after secondary haemorrhage, and in some cases persistent neurological deficits or global brain dysfunction.