Scientists used to think migraines were caused by blood vessels on the surface of your brain dilating and constricting, leading to the pulse of pain people often experienced. They saw migraines as being primarily a vascular disorder. That’s changed. We now know that these changes (and their painful symptoms) are the end result of a more complex nerve pathway in the brain. Today, researchers believe migraines are a neurological disorder that’s largely genetically based. They still don’t understand everything that happens during a migraine, such as why certain symptoms occur—but they are closer to untangling the mystery of the migraine. Here’s what researchers believe happens inside your brain to cause the symptoms you are experiencing. A trigger starts a reaction. First, nerve cells within your brainstem are activated or triggered. This activation can occur for a variety of reasons, including lack of sleep, food or water, for example. A drop in magnesium levels, abnormal calcium channels on the surface of the neuron, mitochondrial changes or other genetic abnormalities are all possible factors. Once activated, the neurons send messages along the trigeminal nerves, a major pain pathway that starts in the brain stem and travels along your face, teeth, eyes, sinuses and forehead, as well as to blood vessels on the surface of the brain. These blood vessels expand or dilate in response. Activity then occurs across the surface of the brain, called a “spreading cortical depression.” This spread moves like a slowly advancing thunderstorm, traveling from the back to the front of your brain. As it passes over the brain, blood vessels constrict, limiting oxygen flow. Researchers believe the cortical depression may be the cause of the visual auras that some people with migraine experience. These auras result in people seeing dark or colored spots, sparkles, or other visual disturbances. Chemicals cause additional symptoms. Your brain also responds to the brainstem activation by releasing chemicals called neuropeptides, including serotonin, noradrenalin, prostaglandins and others. Once released, they travel to the outer layer of your brain–the meninges–which results in inflammation and swelling of blood vessels, causing an increase in blood flow around the brain. This is likely the cause of the throbbing, pulsing pain most people experience during migraine. While the pain may be originating from the surface of your brain, you may feel it in your eyes, temple area, neck, face or sinuses. These neurochemicals also can transmit signals to the part of the brain that controls appetite, nausea and vomiting. Another phenomenon that occurs as a result of this inflammation and chemical interplay is skin super-sensitivity. About 80% of migraine sufferers experience what’s called “cutaneous allodynia” that causes things like earrings, necklaces, neckties and eyeglasses to become painful. Some people say even their hair hurts; this chemical reaction is why. The migraine spreads—then stops. The initial migraine pain that starts with the activation of the neurons in the brainstem changes after about 1 to 2 hours. The migraine then moves to a second stage, where the central nervous system becomes hypersensitive and involved. If you can take medication before the second stage of the migraine occurs, you are more likely to be able to stop the pain. Triptan medication can shut down the initial pain by narrowing the blood vessels and blocking pain transmission. But if the pain cycle continues to the central nervous system, medication becomes less effective. If untreated, migraine can last up to 72 hours, before the nervous system response finally quiets and your brain returns to its normal, pre-activation state.