Pathophysiology of the migraine aura

Migraine auras involve sensory disturbances linked to cerebral cortex disturbances. This suggests that cortical spreading depression (CSD) is a key mechanism. Changes in brain blood flow during migraine attacks support the spreading depression theory. Animal studies have replicated these findings during CSD events. Cortical spreading depression involves a wave of depolarization across the cortex. This wave moves at a rate of 3-5 mm/min. A brief phase of excitation precedes the reaction, followed by nerve cell depression. This occurs alongside a failure in brain ion homeostasis. There is also an efflux of excitatory amino acids from nerve cells. Enhanced energy metabolism accompanies these changes as well. Recent studies show that CSD depends on the activation of the N-methyl-D-aspartate receptor. This receptor is one of three types of glutamate receptors. Combined studies suggest new areas for future migraine treatments and better understanding of attacks. Clinical relevance: Understanding CSD mechanisms may lead to better migraine treatments and management strategies.