Ischemic stroke occurs when a blood vessel supplying blood to the brain is obstructed, leading to a deficiency in oxygen and nutrients essential for neuronal survival. This interruption in blood flow results from a blockage, often caused by a thrombus (blood clot) or an embolus (a traveling clot). The pathophysiology begins with the sudden onset of reduced cerebral perfusion, causing a cascade of metabolic disturbances. Neurons in the affected area experience acute energy failure due to a lack of oxygen and glucose, leading to a breakdown of cellular membranes, release of excitotoxic neurotransmitters like glutamate, and accumulation of intracellular calcium. These processes initiate a cycle of oxidative stress and inflammation, exacerbating neuronal damage. The brain tissue around the core of the infarction enters a state of ischemia but can potentially recover if blood flow is restored promptly. This penumbral zone represents an area of compromised but salvageable tissue. Effective management of ischemic stroke focuses on rapidly restoring blood flow, minimizing the extent of neuronal injury, and preventing secondary complications. Understanding these mechanisms is crucial for developing targeted therapeutic strategies to improve patient outcomes in ischemic stroke.