Migraine is one of the common neurological disorders that presents with unilateral throbbing moderate-to-severe pain and can lead to a significant decrease in quality of life. The increased risk of stroke in patients with migraine, especially those with aura, is well documented in observational studies. The mechanisms linking migraine and stroke are not fully established, but may involve accelerated atherosclerosis, vasospasm, endothelial dysfunction, site-specific induced hypoxemia, and paradoxical embolism. Paradoxical embolism is the entry of thrombus from the venous system and right atrium into the left cardiac system via intracardiac traffic, causing ischemic stroke and embolism of the heart, kidney, and peripheral system. The most common etiology of right-to-left shunts is foramen ovale noncompaction. The frequency of foramen ovale nonocclusion is significantly higher in migraine patients, especially those with migraine with aura. A causal relationship was found between these two relatively common clinical entities. The first supporting evidence is that oval foramen occlusion reduces migraine attacks. In addition, one study found that vasoactive substances (such as serotonin) escape from the pulmonary circulation through the foramen ovale and accumulate in the cerebral vasculature, where vasoactive substances are normally metabolized. These vasoactive substances, may impair cerebral vasomotor reactivity and self-regulation. Reduced cerebral vasomotor reactivity slows the clearance of microemboli, and impaired cerebral vasomotor reactivity may be a mediating mechanism for certain triggers, a mechanism that fills some gaps in the pathophysiology of migraine. It has been demonstrated that the presence of high-grade right-to-left shunts is associated with reduced vasodilatation in migraine patients. The degree of impaired cerebral pressure autoregulation, as quantified by transfer function analysis metrics, is greater in migraine patients if they have larger values of unclosed foramen ovale.