Migraine headaches result from a combination of blood vessel enlargement and the release ofchemicals from nerve fibers that coil around these blood vessels. During the headache, an arteryenlarges that is located on the outside of the skull just under the skin of the temple (temporal artery). This causes a release of chemicals that cause inflammation, pain, and further enlargement of the artery. A migraine headache causes the sympathetic nervous system torespond with feelings of nausea, diarrhea, and vomiting. Migraine headaches have a female predominance with a peak in prevalence in the third and fourth decades of life. Women of reproductive age are liable to develop their first migraine while pregnant or exhibit changes in the character, frequency or severity of their headaches during pregnancy and the puerperium.The purpose of this Review is to examine the pathophysiology underlying the development of migraine headaches and the association of this pathophysiology with pregnancy-related complications. We present the case of a woman with a history of migraine headaches before pregnancy, whose symptoms progressed during pregnancy in part because of increasing exposure to narcotic medications. The abortive medications for moderate or severe migraine headaches are different than OTC analgesics. Instead of relieving pain, they abort headaches by counteracting the cause of the headache, dilation of the temporal arteries. In fact, they cause narrowing of the arteries. Examples of migraine-specific abortive medications are the triptans and ergot preparations. We also discuss the diagnosis and management of migraine headaches that precede pregnancy or develop de novo during pregnancy, placing an emphasis on the distinction between primary migraine headache and headache secondary to pre-eclampsia—a relatively frequent complication of pregnancy and the puerperium. Slot Hoki