Pathophysiology of hemorrhagic stroke
The underlying mechanism of hemorrhagic stroke is the bursting of weakened cerebral vessels and bleeding in the brain. Aneurysms and arteriovenous malformation (AVM) are two conditions that commonly result in the weakening of the vessels.
An aneurysm is a condition characterized by dilation at a point in the blood vessel which is accentuated by high blood pressure. Stretching of the vessel wall causes its thinning which may burst, causing bleeding. An aneurysm is a common cause of subarachnoid hemorrhage.
Brain AVMs are usually congenital in origin. It is a condition in which arteries, carrying oxygenated blood and veins, carrying the deoxygenated blood, form an entangled mesh. This shunts the oxygenated blood directly to the veins and the oxygenation of brain tissue is compromised. These networks are also prone to burst. Each year AVM accounts for 1-3% of brain hemorrhages and has a 20-30% chance of causing permanent brain injury.
In either case, the blood leaked from the vessels tends to pool up in the brain niches, or in between the brain linings depending upon the site of the vessel rupture. The accumulated blood compresses the underlying brain tissue, similarly depriving it of vital nutrients which may eventually cause tissue death.
Older people tend to have another condition called Cerebral Amyloid Angiopathy, in which amyloid protein deposits in the blood vessels, leading to hemorrhages.
The neurons have little to no regenerative potential. This means that it is difficult to revive the brain after tissue death. This property of neurons further potentiate the pathology of stroke.