Pathophysiology of Migraine
The exact pathophysiology of migraine is unclear. It has been suggested that the characteristic pathophysiology of migraine is the cortical spreading depression (CSD) of neural impulses from a focal point of vasoconstriction followed by vasodilation. However, it is unlikely that vasoconstriction followed by vasodilation (spreading depression) or vasodilation alone accounts for the local edema and focal tenderness often observed in migraine patients.[8,10] Lashley described the progressive nature of the visual aura in 1941. Leao described spreading depression in 1944. Milner connected these two developments in 1959. The work of Moskowitz and Olesen was seminal in our current understanding of spreading depression in migraine.[19,20] The relation of migraine to arteries is still an important part of the pathophysiology. A central generator in the hypothalamus or periaqueductal gray has not been ruled out. In migraine patients, the spreading depression passing through nerve cells stimulates the release of several endogenous substances that cause inflammation, makes nerve fibers more sensitive to pain and causes vasodilation.[21,22] There are at least two theories of migraine headaches, including vascular theory and neural theory (Figure 1).
An overview of the pathogenesis of migraine headache. According to vascular theory, vascular disturbances (vasodilatation–vasoconstriction) lead to migraine attacks through a cascade involving inflammation and the serotonin system. According to neural theory, hyperexcitability in the form of cortical spreading depression leads to migraine through a cascade involving inflammation and the sympathetic nervous system. There are alternative theories that may overlap with key mechanisms that may activate neural inflammation and lead to migraine pain.
Expert Rev Clin Pharmacol. 2013;6(3):271-288. © 2013 Expert Reviews Ltd.