What causes migraine headaches?
The short answer is, no one really knows. Despite the fact that between 10 and 20%
of the population—some 30 million people in the United States alone—suffer from migraine
headaches, the exact mechanisms within the brain that give rise to the intolerable pain of
migraine are still not precisely identified. Several conflicting theories make it clear that
migraine headaches are a complex process.
The best-known theory about migraines is more than fifty years old. It holds that migraines are caused by spasms in the vessels supplying blood to the brain. Cerebral blood vessels are lined with muscles that allow them to constrict (narrow) and dilate (widen) to maintain a stable blood supply to the fragile brain tissue.
For unknown reasons, the muscle cells within the vessels spasm, causing constriction, then relax and dilate. Migraine auras occur during constriction, and the pain of migraine occurs when the vessels dilate.
The blood vessels that supply the meninges (a membrane that covers the entire surface of the brain and spinal cord) are well supplied with nerves. When blood vessels in the meninges dilate, the nerves (trigeminal sensory nerves) are stimulated. Pain is the result. Nerve stimulation causes the release of brain chemicals (neuropeptides) that increase dilation—and pain—even more.
Brain dysfunction theories
While the constriction and dilation of brain blood vessels during migraine attacks is well documented, more current theories hold that the patterns of blood flow change as a result of other problems with the brain's function.
Very weak bioelectrical charges are the basis of the brain's activity. Normally, when neurons (nerve cells) in the brain are at rest, they have a slightly different electric charge from the microscopic spaces that surround them. When a nerve cell ‘fires,' this charge instantaneously shifts and is then quickly restored to normal.
‘Depolarization' means that the normal resting bioelectrical charges of nerve cells in the brain are disrupted. This theory holds that a brief wave of depolarization spreads from the back to the front of the brain, during which neurons become much more prone to fire. This is followed by a much longer period of depressed neuron function, which causes changes in blood flow in the brain.
According to this theory, sensory auras happen during the depolarization phase, as neurons fire more easily. The depressed phase that follows brings the pain of migraine.
Serotonin is one of the brain's main neurotransmitters—chemicals that act as signals for neurons. According to the serotonin theory, disruptions in the brain's normal chemistry cause migraine headaches.
Lab studies of people undergoing migraines document variations in serotonin levels during an attack. Serotonin levels initially increase, which constricts the blood vessels and reduces blood flow in the brain enough to cause an aura. Serotonin levels in the brain then decrease as the supply of this neurotransmitter is used up, causing dilation—and migraine pain.
One particular structure in the brain stem (the most primitive part of the brain, located just above the spinal cord) is very sensitive to brain serotonin levels. It's called the ‘dorsal raphe nucleus,' and many of its neurons both secrete serotonin and intertwine with cerebral blood vessels, allowing the serotonin to directly affect the vessels. Part of the serotonin theory of migraines is that the dorsal raphe nucleus may function as a ‘migraine generator,' triggering the constriction and dilation of blood vessels.
The neurovascular theory suggests that either migraine triggers or a wave of depolarization activates the trigeminal nerve cells that supply the blood vessels of the meninges. The neurons release chemicals that cause the vessels to dilate and also create inflammation around them. The inflammation is the cause of pain. The inflammation further activates the trigeminal nerve, increasing the pain.
According to this theory, vasodilation is a result of nerve activation, not the cause of migraine headache. In people who suffer from migraines, the trigeminal nerve is believed to be more likely to be activated than it is in people without migraines.
The hypothalamus is an almond-sized gland located deep within the brain; it's a central regulator of neurotransmitters (chemicals that activate neurons) and hormones. The most recent theory of migraine holds that abnormal functioning of the hypothalamus causes migraine headaches, as well as the auras that precede them. Several studies have shown abnormal activity in the hypothalamus among migraine sufferers, compared to the general population. This theory tends to be supported by other experiences that people with migraines have—like sleep disturbances—that can also be caused by abnormal functioning of the hypothalamus.
It can be deeply frustrating to suffer from so much pain for no known reason. However, one thing these theories all make clear is that some part of the brains of migraine sufferers—whether it's the hypothalamus, the trigeminal nerve, the blood vessels, or the dorsal raphe nucleus—is distinctly different from the brains of people who don't have migraines.