Abstract
Central (cortex and upper brainstem) and peripheral (trigeminovascular) mechanisms are involved in the pathophysiology of migraine. We propose that unknown migraine triggers initiate depolarization of cortical neurons followed concomitantly by a transient increase in blood flow. This transient hyperemia spreads at a rate of 3-6 mm/min followed by hypoperfusion which is more long-lasting. Through unknown mechanisms (probably chemical), we hypothesize that this wave activates or sensitizes trigeminovascular axons which is a consequence of neuropeptide release and neurogenic inflammation. Orthodromic conduction along trigeminovascular fibers transmits information centrally via the trigeminal caudalis and other brainstem nuclei to higher cortical structures for registration and modulation of nociceptive information.
