At the cellular level, a stroke initiates a complex cascade of events that culminates in cellular injury and, ultimately, irreversible damage. In ischemic strokes, where blood flow to a part of the brain is obstructed, the initial deprivation of oxygen and nutrients triggers cellular energy failure. Without sufficient energy, vital cellular processes stop, leading to dysfunction and, eventually, cell death. Additionally, the lack of oxygen prompts neurons to release excitatory neurotransmitters excessively, a phenomenon known as excitotoxicity. This surge of excitatory signals exacerbates cellular damage and initiates a series of inflammatory responses. Inflammation further compounds the injury, as immune cells infiltrate the affected area, releasing pro-inflammatory cytokines and worsening tissue damage. Additionally, the breakdown of cell membranes during stroke leads to the release of toxic molecules, contributing to neuronal death and the formation of harmful reactive oxygen species. Overtime, the ongoing inflammation and stress from harmful molecules continue to damage cells, spreading the harm even further beyond the initial injury. In hemorrhagic strokes, the presence of blood in the brain surrounding tissues triggers a different set of cellular responses. This excess of blood exerts physical pressure on adjacent brain cells, disrupting their normal function and impeding blood circulation. Furthermore, the breakdown products of blood, such as hemoglobin and iron, induce oxidative stress and inflammation, exacerbating cellular injury in the surrounding tissue. Collectively, these cellular events are what makes it of the utmost importance to act promptly in stroke interventions to limit brain damage and optimize patient outcomes.