Abstract

There is clinical experimental evidence that extracranial arterial vasodilation, extracranial neurogenic inflammation, and decreased inhibition of central pain transmission are involved in the pathogenesis of the migraine headache. The migraine aura is likely caused by a neurophysiologic phenomenon akin to Leão's cortical spreading depression, a wave of short-lasting neuronal excitation that travels over the cerebral cortex, followed by prolonged depression of cortical neuronal activity. A concept of the pathogenesis of the migraine attack is presented, in which the relation of the mechanism of the migraine aura and that of the migraine headache is considered parallel rather than sequential in nature. The process driving the pathogenesis of the migraine attack and susceptible to the migraine trigger factors may be located in the brain stem.

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