The pathophysiology of migraine is not fully understood. Recent studies have shed light on the neuronal events mediating the aura and headache phases of migraine. Cortical spreading depression appears to underlie the aura phase in patients with migraine with aura, and it may also precede headache in patients with migraine without aura. Recent evidence suggests that the pain of the headache phase is mediated by the trigeminal vascular system and its central projections. The trigeminal afferents project centrally to the caudal brainstem nucleus caudalis and to the dorsal horn of the cervical spinal cord. Additional cortical, thalamic, and brainstem regions are also activated during migraine. In a clinical study of patients with spontaneous migraine, increased blood flow to the rostral brainstem but not to cortical areas persisted after the pharmacologic relief of headache, suggesting that the rostral brainstem may contain candidate regions for a migraine generator. It is currently thought that the neuronal mechanisms underlying headache may function similarly in healthy and migrainous individuals, but because of a central neuronal hyperexcitability in patients with migraine, headache is more easily triggered in these individuals.
|Original language||English (US)|
|Issue number||7 SUPPL. 2|
|State||Published - Apr 8 2003|
ASJC Scopus subject areas
- Clinical Neurology