Following its entrance into the human body through inhalation, carbon monoxide (CO) forms carboxyhemoglobin (COHb) by binding to hemoglobin (Hb) within the blood. Massive ischemic tissue necrosis occurs in 0.5%-1% of cases with CO poisoning. [1] The affinity of CO to Hb is 200-250 times more when compared to the affinity of oxygen. As a result of CO binding to Hb, oxygen delivery to the tissues is reduced, and tissue hypoxia develops. This affects mostly the brain and heart, which are the organs with the highest demand for oxygen. Hypoxia leads to oxidative stress, cellular necrosis, apoptosis, and inflammation in acute CO poisoning. Pathological changes in the brain observed in CO poisoning are hippocampal necrosis, demyelination of the cerebral white matter, and spongy necrosis of the globus pallidus and cerebral cortex. [2] In this report, we aim to present our two cases where ischemic stroke developed following CO poisoning.