Figure 2.

Stroke pathophysiology. The clot formation process starts with disrupting the blood–brain barrier due to a rupture of the endothelial cell layer, exposing the blood vessel's inner collagen layer. Collagen exposure is recognized by circulating platelets in the bloodstream, which initiates the process of aggregation. Fibrinogen is released from the liver to the bloodstream and is cleaved by thrombin at the damaged site, resulting in fibrin formation. Fibrin is one of the main constituents of blood clots, providing remarkable biochemical and mechanical stability. The blood clot is also composed of neutrophils and leukocytes that arrive at the injured site and form a solid structure that obstructs or reduces blood flow. The reduction in blood flow leads to a decrease in oxygen and glucose levels. These conditions favor a shift in the neuron's metabolic conditions, mitochondrial dysfunction, excitotoxicity, ion imbalance, and neuronal death. Figure was drawn using Biorender.com.