What is stroke?

A stroke, also known as a cerebrovascular accident (CVA), occurs when the blood supply to part of the brain is disrupted or reduced, leading to damage or death of brain cells. Strokes can be ischemic, caused by blockage or narrowing of a blood vessel in the brain, or hemorrhagic, caused by bleeding into the brain tissue. Strokes are a medical emergency and require immediate medical attention to minimize brain damage and prevent complications.


There are two main types of strokes:


  • Ischemic Stroke: This type of stroke occurs when a blood clot or plaque buildup blocks or narrows an artery supplying blood to the brain. Ischemic strokes account for the majority of strokes and can result from various conditions, including atherosclerosis (hardening and narrowing of the arteries), blood clots originating from the heart or blood vessels, or emboli (clots or debris traveling through the bloodstream).


  • Hemorrhagic Stroke: This type of stroke occurs when a blood vessel in the brain ruptures or leaks, leading to bleeding into the surrounding brain tissue. Hemorrhagic strokes can be caused by conditions such as hypertension (high blood pressure), aneurysms (weak spots in blood vessel walls), arteriovenous malformations (abnormal tangles of blood vessels), or trauma.


What is the relationship between stroke and oxidative stress?

The relationship between stroke and oxidative stress is significant and plays a crucial role in the pathophysiology of stroke-related brain injury. Here’s how stroke contributes to oxidative stress:


  • Ischemia-Reperfusion Injury: In ischemic stroke, the initial reduction or cessation of blood flow to the brain (ischemia) leads to a decrease in oxygen and nutrient supply to brain cells. This deprivation of oxygen and glucose triggers a cascade of biochemical reactions, including the production of reactive oxygen species (ROS) as a byproduct of cellular metabolism. When blood flow is restored (reperfusion) through treatments such as thrombolytic therapy or mechanical thrombectomy, the sudden influx of oxygen-rich blood can exacerbate oxidative stress by promoting the generation of additional ROS.


  • Mitochondrial Dysfunction: Ischemic stroke disrupts mitochondrial function within brain cells. Mitochondria are the primary producers of energy (ATP) in cells but are also a major source of ROS generation. The disruption of mitochondrial electron transport chains during ischemia-reperfusion leads to the overproduction of ROS, contributing to oxidative stress and cellular damage.


  • Inflammatory Response: Stroke triggers an inflammatory response in the brain, characterized by the activation of immune cells and the release of pro-inflammatory cytokines and chemokines. Inflammatory cells, such as microglia and infiltrating leukocytes, generate ROS as part of their antimicrobial and tissue repair functions. However, excessive inflammation can lead to the overproduction of ROS and exacerbate oxidative stress in the brain.


  • Blood-Brain Barrier Dysfunction: Ischemic stroke disrupts the integrity of the blood-brain barrier (BBB), a specialized structure that regulates the movement of molecules between the bloodstream and the brain. BBB dysfunction allows the infiltration of inflammatory cells and plasma components into the brain parenchyma, further amplifying the inflammatory response and oxidative stress.


  • Excitotoxicity: Ischemic stroke leads to the excessive release of excitatory neurotransmitters, such as glutamate, which can trigger neuronal hyperexcitability and calcium overload. Calcium influx into neurons activates enzymes like nitric oxide synthase and NADPH oxidase, leading to the production of ROS and oxidative stress.


Overall, oxidative stress plays a critical role in the progression of brain injury following stroke, contributing to neuronal death, blood-brain barrier disruption, and neuroinflammation.