The Pathophysiological and Pharmacological Basis of Current Drug Treatment of Migraine Headache

Doodipala Samba Reddy

Disclosures

Expert Rev Clin Pharmacol. 2013;6(3):271-288. 

In This Article

Vascular Theory

Wolff first developed the vascular theory (vascular disturbances) of migraine in the 1940s.[17] Migraine attacks are believed to be initiated by vasoconstriction in the cranial blood vessels, leading to oligemia and reduction in blood flow. Reduced cerebral blood flow is thought to initiate a cascade and generate an aura. Compensatory vasodilation occurring in intracranial or extracranial blood vessels after vasoconstriction is assumed to result in perivascular edema and inflammation. This may ultimately trigger migraine headache. A substantial area of the brain is insensitive to pain but meningeal blood vessels are richly innervated by pain fibers. Blood vessel dilation is believed to stimulate the trigeminal sensory nerves that surround the meningeal blood vessels, thereby leading to pain. It has been suggested that 5-hydroxytryptamine (5-HT, or serotonin) is a key mediator in the pathogenesis of migraine, especially the vascular component of migraines. This is consistent with the high efficacy of 5-HT-receptor agonists for acute treatment of migraine headaches. However, there is some debate and controversy because vascular changes are not consistent with the temporal pain events. Clinical studies, however, have demonstrated a lack of correlation between the changes in blood flow and migraine symptoms.[23] These observations raised skepticism about the vascular etiology of migraines. Such observation has led to studies on the neural theory.

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