Despite numerous theories on the pathogenesis of migraine, the exact site of origin of a migraine attack remains unknown. Although most attention has been directed toward the peripheral nervous system, the central nervous system plays an important though incompletely understood role. There are a variety of types of migraine, but similar mechanisms seem to operate in all variants. Based on present evidence, the symp-, toms of migraine are related to a disturbance of the central vasomotor centers, the extracranial and intracranial blood vessels, and the microcirculation.1,2 Each attack represents an initial phase of arterial vasoconstriction, largely intracranial, and associated with a slowly spreading process of cortical depression accounting for the slow progressive march of neurological symptoms, followed by a phase of painful arterial vasodilatation with increased blood flow of the extracranial or scalp arteries associated with a localized "sterile inflammation" of the arterial wall. However, this traditional view that
Friedman AP. Part 1: Migraine Headaches. JAMA. 1972;222(11):1399–1402. doi:10.1001/jama.1972.03210110039009
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