A series of biochemical changes occur in the fashion of migraine attacks. During the aura phase, plasma 5-hydroxytryptamine (5-HT) levels may be transiently increased; the metabolite of 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), may be significantly increased in the urine during a headache attack. This suggests that plasma 5-HT is quickly degraded and excreted from the urine. 5-HT has a biphasic effect on smooth muscle, with a decrease in plasma 5-HT causing constriction of small arteries and dilation of larger arteries. Constriction of small arteries causes ischemia in brain tissue, producing aura or other symptoms of neurological damage; dilation of large arteries causes headache. Some of the 5-HT leaks into the extracellular fluid surrounding the blood vessels, and together with histamine, bradykinin, vasopressin, and other neuropeptides, it decreases the pain threshold of the vessel wall and causes “sterile inflammation” of the arteries. The combination of vasodilatation and “sterile inflammation” causes the clinical symptoms of migraine. 5-HT is mainly stored in platelets, and when platelet aggregation is increased or 5-HT releasing factors are present, the platelet 5-HT content suddenly decreases and clinical onset occurs. Certain drugs (e.g., reserpine) have a 5-HT releasing and depleting effect and can induce headache attacks in migraine patients; 5-HT blockers (e.g., dimethyl ergometrine, phenothiazine) are used to prevent migraine attacks. Decreased monoamine oxidase (MAO) activity during headache attacks may be related to the consumption of large amounts of MAO during 5-HT degradation. Treatment is taken, vascular nerve decompression, with good results and high cure rate.