Migraine is a spectrum disease, usually manifesting as an episodic or chronic primary headache disorder, characterized by attacks that can last from a few hours to up to three days. It is two to three times more prevalent among women than men, and women experience higher levels of pain, longer lasting attacks, and greater disability than men. For much of the twentieth century, migraine’s causes were considered to be vascular, and the pain a result of dilation of the cranial blood vessels. Since the 1970s, the emphasis has shifted, and it is now defined as a disorder involving nerve pathways and chemicals in the brain, to which people are often genetically predisposed. While migraine is still understood to affect the neurovascular system, it seems likely that the headache pain comes from neurogenic inflammation, rather than vasodilation. This is a problem of brain function, rather than structure. As the website for the National Migraine Centre in London explains, “if the brain is a computer, migraine is a software not a hardware problem.” Nevertheless, a huge amount remains unknown, including the role of the hypothalamus (the part of the brain that controls the endocrine system and has a role in the menstrual cycle, pain modulation, and governance of the body’s circadian rhythms), the cause of premonitory symptoms, the extent to which antimigraine drugs can access the brain, and the role of the blood-brain barrier.