A stroke is a medical emergency where the brain’s blood flow is interrupted or significantly reduced, depriving brain tissue of oxygen and nutrients. This leads to brain cell damage or death within minutes. Understanding its pathology helps grasp the full impact of a stroke on the brain and body.
Understanding Stroke Types
Strokes primarily fall into two categories. Ischemic strokes, about 87% of cases, occur when a blood vessel supplying the brain becomes blocked. This blockage, often a blood clot (thrombus) from atherosclerosis or an embolus from elsewhere, restricts blood flow and oxygen to brain tissue.
A Transient Ischemic Attack (TIA) is a temporary disruption of blood flow, sharing the same underlying blockage as an ischemic stroke. TIA symptoms usually resolve within minutes to an hour and typically do not cause permanent brain damage. However, TIAs serve as a warning sign for a future stroke and require immediate medical evaluation.
Hemorrhagic strokes, about 13% of cases, result from a ruptured blood vessel causing bleeding into or around the brain. This bleeding can occur within brain tissue (intracerebral hemorrhage) or between the brain and its membranes (subarachnoid hemorrhage). Accumulated blood directly damages brain cells, creates pressure on surrounding tissue, and disrupts normal blood flow.
Mechanisms of Brain Damage
After blood flow interruption or bleeding, a complex cascade of cellular and molecular events leads to widespread brain damage. One mechanism is excitotoxicity, where excessive glutamate overstimulates neurons. While glutamate normally aids brain function, its uncontrolled release during stroke causes an abnormal influx of calcium ions into neurons, activating destructive enzymes that damage cellular components and ultimately cause cell death.
Oxidative stress also contributes to brain injury, arising from an imbalance between reactive oxygen species (ROS), or free radicals, and the brain’s ability to neutralize them. The brain is vulnerable to oxidative damage due to its high metabolic activity and low levels of protective antioxidants. These reactive species damage cellular components like lipids, proteins, and DNA, leading to cellular dysfunction and death.
Inflammation is another contributor to secondary brain damage after a stroke. The brain’s immune response involves the activation of resident immune cells, primarily microglia and astrocytes. These activated cells release pro-inflammatory mediators like cytokines and chemokines, which can exacerbate neuronal damage, compromise the blood-brain barrier, and recruit additional immune cells. While acute inflammation aids in clearing damaged tissue, prolonged or excessive inflammation can lead to further harm to brain tissue.
Brain cells primarily die through two distinct processes: apoptosis and necrosis. Necrosis, often seen in the infarct core where blood flow is severely cut off, involves rapid, uncontrolled cell swelling and bursting, leading to an inflammatory response. Apoptosis, or programmed cell death, is a more orderly process that can occur in the surrounding “at-risk” penumbra, hours or days after the stroke. This process involves DNA fragmentation and protein degradation, contributing to significant tissue loss.
Brain swelling, or cerebral edema, is a common and serious stroke complication. Edema is classified as cytotoxic, where cells swell due to ion imbalance, and vasogenic, involving fluid leakage from damaged blood vessels due to blood-brain barrier disruption. This fluid accumulation increases pressure within the rigid skull, compressing brain tissue, further compromising blood flow, and potentially leading to life-threatening herniation.
Immediate Consequences of Brain Damage
After a stroke, the brain experiences immediate impacts on its structure and function. The damaged area is typically divided into two zones: the infarct core and the ischemic penumbra. The infarct core is where blood flow is so severely reduced that tissue damage is irreversible.
The ischemic penumbra surrounds this core. This brain tissue is functionally impaired by reduced blood flow but remains metabolically active and potentially salvageable if blood flow is restored promptly. Acute stroke intervention aims to prevent this penumbra from progressing to irreversible infarction.
Damage to neurons and their intricate connections directly disrupts neural networks. This disruption leads to immediate functional deficits, as the brain’s ability to process information, coordinate movements, and communicate effectively is compromised. The extent of these deficits depends on the location and size of the damaged brain region.
Increased intracranial pressure (ICP) is a common and serious consequence of brain damage. As brain tissue swells due to edema, pressure inside the skull rises, which can further reduce blood flow to the brain and lead to additional tissue damage. Even a moderate ICP increase can significantly reduce blood flow through collateral vessels, which are alternative pathways for blood supply.
The blood-brain barrier (BBB) is frequently compromised after a stroke. This specialized barrier normally protects the brain from harmful substances, but its disruption allows potentially toxic blood components to enter brain tissue. BBB breakdown can worsen brain edema and contribute to hemorrhagic transformation, where an ischemic stroke converts into a hemorrhagic one, further complicating the injury.
Pathological damage and subsequent brain changes manifest as immediate neurological symptoms. These include sudden weakness or paralysis, often affecting one side of the body, and difficulties with speech, such as slurred words or trouble understanding language. Other symptoms may involve problems with vision, dizziness, confusion, or a sudden, severe headache, depending on the affected brain area.