Migraine is an episodic disorder, the centerpiece of which is a severe headache generally associated with nausea, and/or light and sound sensitivity. It is one of the most common complaints encountered by neurologists in day to day practice.
The pathophysiology, clinical manifestations, diagnosis, and complications of migraine will be reviewed here. Other aspects of migraine are discussed separately. (See "Acute treatment of migraine in adults" and "Preventive treatment of migraine in adults" and "Chronic migraine" and "Migraine with brainstem aura (basilar-type migraine)" and "Hemiplegic migraine" and "Vestibular migraine" and "Headache, migraine, and stroke".)
The current state of knowledge suggests that a primary neuronal dysfunction leads to a sequence of changes intracranially and extracranially that account for migraine , including the four phases of premonitory symptoms, aura, headache, and postdrome.
The once popular vascular theory of migraine, which suggested that migraine headache was caused by the dilatation of blood vessels, while the aura of migraine resulted from vasoconstriction, is no longer considered viable [2-4]. Vasodilatation, if it occurs at all during spontaneous migraine attacks , is probably an epiphenomenon resulting from instability in the central neurovascular control mechanism .
Cortical spreading depression — A causal association between migraine aura and headache is supported by evidence that both are linked to the phenomenon known as cortical spreading depression of Leão [2,6,7]. Cortical spreading depression is a self propagating wave of neuronal and glial depolarization that spreads across the cerebral cortex. Cortical spreading depression is hypothesized to: