The foramen ovale is a slit-like valve between the septum primum and septum secundum that exists in the mammalian fetal heart. This valve opening provides a right-to-left heart shunt so that oxygenated blood from the placenta can bypass the pulmonary circulation and flow directly to the fetal brain. After birth, the two septa fuse to complete the separation of the left and right atria but the foramen ovale remains patent in about 20% of the adult population.1 This defect was thought to be of little clinical significance; however, patent foramen ovale (PFO) has recently been implicated in several diseases, including PLATYPNEA–ORTHODEOXIA SYNDROME and neurologic decompression illness in scuba divers, and case–control studies have indicated a role in cryptogenic stroke.1 These conditions are believed to occur when the PFO allows right-to-left shunting of blood associated with arterial desaturation, nitrogen bubbles or blood clots. Cryptogenic stroke describes a neurologic deficit that has no identifiable cause. One of the theoretical causes for such an event is paradoxical embolism—a small clot that bypasses the pulmonary circulation and enters the systemic circulation, where it lodges in the brain. This proposed mechanism would support the theory that people with a PFO have increased stroke risk.2 Recently, PFO has received attention for its possible association with migraine headaches. In this Viewpoint, we discuss the possibility that the majority of migraine headache could be treated by closing the PFO passageway through the heart.
Migraine headaches are a debilitating condition experienced by 12% of the general population. Remarkably, up to 48% of patients presenting with cryptogenic stroke report a history of migraine headaches.3 For 20% of individuals with migraines, these headaches are accompanied by an AURA. While the neurologic pathways of migraine activity in the brainstem and cortex have been examined extensively, little is known about the mechanisms that trigger migraines with or without aura. Patients with migraine headache have a 60% incidence of cardiac or pulmonary right-to-left shunts, primarily because of PFOs. On the basis of PFO physiology and increased association, it is thought that a subset of migraines might be precipitated by substances that can pass through a PFO. According to this theory, compounds that are normally metabolized or diluted by the lungs could cause migraine headaches when shunted directly into the cerebral circulation via a PFO. An alternative theory suggests that migraines associated with PFO are triggered by small venous emboli. It is known that patients with migraine headaches have an increased risk for stroke compared with the general population and that there is a 13-fold increase in the incidence of MRI abnormalities in these patients compared with matched controls.4 In the past, it was believed that intense cerebral arterial spasm induced the migraine and that arterial dilation was responsible for the throbbing headache; if the initiating arterial constriction were intense enough, it could produce a stroke. These days a migraine is considered to be a neurovascular disorder, in which the primary event manifests in the cerebral cortex as a spreading wave of neuronal depression, with subsequent arterial constriction and decreased blood flow to the posterior circulation. We believe that migraine-associated stroke is another manifestation of cryptogenic stroke that occurs when venous emboli bypass the lungs via a PFO and enter the brain.2
This is a preview of subscription content, access via your institution
