This article discusses the basic mechanisms of migraine aura and its clinical significance based upon evidence from human studies and animal models.
Prospective clinical studies have reinforced the understanding that migraine aura is highly variable from one individual to the next as well as from attack to attack in an individual. While migraine with aura clearly has a higher heritability than migraine without aura, population studies have not identified specific genes that underlie this heritability for typical migraine with aura. Imaging studies reveal hypoperfusion associated with migraine aura, although the timing and distribution of this hypoperfusion is not strictly correlated with migraine symptoms. Mapping of migraine visual aura symptoms onto the visual cortex suggests that the mechanisms underlying the aura propagate in a linear fashion along gyri or sulci rather than as a concentric wave and also suggests that aura may propagate in the absence of clinical symptoms. Cortical spreading depression in animal models continues to be a translational model for migraine, and the study of spreading depolarizations in the injured human brain has provided new insight into potential mechanisms of cortical spreading depression in migraine. Migraine with aura has multiple comorbidities including patent foramen ovale, stroke, and psychiatric disorders; the shared mechanisms underlying these comorbidities remains a topic of active investigation.
Although it occurs in the minority of patients with migraine, aura may have much to teach us about basic mechanisms of migraine. In addition, its occurrence may influence clinical management regarding comorbid conditions and acute and preventive therapy.