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What Causes A Headache?
By: Stephen D. Silberstein, M.D.
You may say, "I know what causes my headaches. Staying up late or drinking too much coffee will bring on a headache every time." But a trigger is not the same as a cause. Aged cheese, cigarette smoke, alcohol, excessive caffeine, bright sunlight, disrupted sleep patterns, and many other factors can trigger headaches in some migraine- or headache-prone patients. However, even a known trigger does not always lead to a headache. Therefore, these factors cannot be said to be a cause of headache the way a particular virus is the cause of a head cold or flu. Instead, the nervous system of the headache sufferer is somehow predisposed to respond to these triggers and other stresses with a series of biochemical changes that result in the pain and other symptoms of headache.
Until recently, medical researchers believed that tension-type headache was caused by contraction of muscles of the head and neck, and that migraine headache resulted from the expansion (or dilation) of blood vessels in the brain and scalp. The migraine aura was thought to be due to a constriction of the blood vessels, which preceded the dilation and which reduced blood supply to the eyes and brain. These theories made sense to both physicians and patients, since they accounted for the tenderness and the throbbing experienced with these forms of headache, as well as the visual disturbances of aura. However, the vascular (involving blood vessels) theory could not explain many of the other symptoms of migraine, including the mood changes before and after the attack, and the nausea and vomiting that occur during the attack.
The use of new noninvasive technology, such as MRI, PET and CT scans, along with the great advances in understanding the brain's biochemistry, have taught us much more about the causes of head pain. As we now know, vascular changes may be an important factor in a headache attack, but they are not the whole story nor the root cause. A reduction in brain activity, rather than blood supply, seems to be linked to the migraine aura. Similarly, there is little evidence that muscle contraction causes tension-type headache. Some researchers think that several stages in the complex pain-producing process are similar for these two distinct headache disorders.
The brain and the nerves communicate by means of a special group of chemicals called neurotransmitters. The neurotransmitters are essential for all nervous system functioning, including muscle contraction, sensory perception, thought, mood, and awareness of pain. No single neurotransmitter regulates processes so complex as mood and pain perception. Moreover, each neurotransmitter can have multiple roles throughout the brain and nervous system--as if the same chemical "word" had different definitions in different organs. In migraine, changes in the availability of a particular neurotransmitter called serotonin seems to be the most important single event in causing an attack.
Serotonin is known to affect sleep, mood, blood vessel elasticity (constriction and expansion), and contraction of smooth muscles, such as those of the gut. It also regulates the release of another neurotransmitter called "substance P," which increases the permeability of capillaries, so that substances leak into surrounding tissue. This local leakage (edema) includes release of an irritating and inflammatory chemical called bradykinin, which stimulates the pain-conducting nerves. At the same time, substance P is one of the most powerful facilitators of pain. It makes the pain-conducting nerve fibers more sensitive to the presence of bradykinin and to substance P itself. This suggests there are two aspects to the head pain--a "double whammy." The vascular changes may be a source of pain, but sensitivity to pain has been greatly increased by the action of substance P and bradykinin.
This does not mean that headache sufferers have "a low pain threshold"--a simplistic view of pain that implies personal weakness. Pain perception depends upon the balance of activity of chemicals that decrease or inhibit pain awareness, such as the endorphins, and chemicals that increase or facilitate it, such as substance P and bradykinin. If substance P is being released and taken up by the pain-conducting nerves, you can't help feeling pain any more than you can help hearing a firecracker explode near your ear. Incidentally, the brain itself is insensitive to pain. The pain-sensitive parts of the head are the scalp and its blood supply, the head and neck muscles, the nasal sinuses, some of the arteries of the brain, the lower portion of the membrane surrounding the brain (the dura mater), and some of the neck and brain nerves.
The serotonin theory of migraine also provides an explanation for the mood changes (irritability, depression, or sometimes elation) than many sufferers experience before and/or after an attack. A second neurotransmitter, norepinephrine (noradrenaline), also plays a role in pain perception during migraine. In addition, the female hormone estrogen is known to be involved in migraine, possibly by stimulating prostaglandins, which also cause blood vessels to constrict and dilate.
Theories are useful. The serotonin theory of migraine, however incomplete it may be, has helped explain how some classes of migraine medication work (such as antidepressants), and has guided efforts to develop more effective ones. Sumatriptan was designed to have a specific effect on part of the serotonin system. DHE, another headache drug, has also been shown to affect the serotonin system. Sumatriptan's predicted success in treating migraine and its unexpected usefulness for other types of headache gives us important clues to refining our theories of headache. In turn, a more accurate and complete theory can direct the design of more effective medications with fewer side effects.
(Stephen D. Silberstein, M.D., Co-Director, Comprehensive Headache Center, The Germantown Hospital and Medical Center, Philadelphia, PA)