Bridging the Gap: Translating Microemboli-Induced Spreading Depolarization Into Clinical Practice

A 68-year-old woman developed daily episodes of migraine aura following mitral valve surgery. During aura symptoms, microemboli in the posterior circulation were detected in real time by transcranial Doppler. After initiation of antiplatelet therapy, the daily clinical episodes ceased, and microemboli were not detectable on repeated transcranial Doppler. Spreading depolarization, the underlying mechanism of migraine aura symptoms, is a conserved electrophysiologic phenomenon characterized by a propagating wave of neuronal and glial depolarization. Experimental models demonstrate that spreading depolarization can be triggered by cortical ischemic lesions and by air emboli, cholesterol crystals, or microspheres in the cerebral circulation without apparent tissue injury. This case illustrates cerebral microembolism-triggered clinical episodes suggestive of cortical spreading depolarization. We therefore suggest that transient neurologic episodes with the characteristics of cortical spreading depolarization, that is, sequential, retinotopically or somatotopically spreading, neurologic symptoms with positive features, can be induced by microembolism in humans.