Abstract
The article summarizes the current understanding of the pathophysiology of migraine. Some controversial aspects of the underlying mechanisms of the disorder are mentioned.
In general, five phases of migraine are recognized: prodromal, aura, headache, postdromal, and interictal. These phases may overlap or may not occur from attack to attack or from person to person.
In the article, pathophysiologic mechanisms of individual phases are discussed. Character of clinical symptoms and recent functional neuroimaging studies focusing on the prodromal phase of migraine support the role of the hypothalamus in this phase.
Altered sensory processing during the interictal and prodromal phase may contribute to the development of a migraine attack. Indirect evidence supports the generally accepted hypothesis that the pathophysiological mechanism of aura is cortical spreading depolarization.
Headache is mediated by the activation of the trigeminovascular system (pathway). The release of calcitonin gene-related peptide plays the key role here.
Brain regions and mechanisms responsible for the prodromal phase could also play a role in the postdromal phase. Migraine can be seen as a complex cyclical brain disorder that likely results from dysfunction of more brain areas and their connections.