During the painful phase of attacks of vascular headache of the migraine type there is dilatation of the large and small blood vessels of the head both intra- and extracranially, often more on one side than the other.1-3 In most attacks, however, the pain stems chiefly from the large subsurface cranial arteries and their branches. Aching pain is experienced when these vessels are distended, pulled upon, or displaced. Yet dilatation of these vessels, for instance that induced by immersion of the body in hot water, is not usually painful and does not induce other focal features of the migraine attack, i.e., edema, tenderness on pressure, and heightened vulnerability of tissue to injury. These observations led to the hypothesis that in addition to vasodilatation, a local sterile inflammation occurs. Also a substance (or substances) accumulates in the walls of the arteries and in the adjacent perivascular, areolar, and supporting tissues
CHAPMAN LF, RAMOS AO, GOODELL H, SILVERMAN G, WOLFF HG. A Humoral Agent Implicated in Vascular Headache of the Migraine Type. Arch Neurol. 1960;3(3):223–229. doi:10.1001/archneur.1960.00450030001001
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