About 15% of migraine sufferers have a warning that the headache is coming on. They experience a change in brain function called an aura. It is usually a visual symptom, such as an arc of sparkling (scintillating) zig-zag lines or a blotting out of vision or both. But any other brain-related symptom may occur, such as numbness of one side of the face and hand, weakness, unsteadiness, or altered consciousness. In past years these symptoms were thought to be caused by spasm of blood vessels supplying parts of the brain, and the headache was thought to be due to subsequent expansion (dilation) of blood vessels in the head. We now know that it is not that simple.
In an earlier issue (vol. 6, no. 2), we discussed the cause of the pain, of migraine headache. Headache follows certain changes that take place in the nerves to the major blood vessels in the head. The aura is due to changes that take place in the cortex, the outer layer of the brain.
The nerve cells of the brain are always active. This can be seen by the electrical activity they generate on the electroencephalogram (EEG). In experiments with animals, the EEG shows a depression (lowering) of nerve cell activity below a spot on the cortex of the brain that has been stimulated. Surrounding the area of depressed activity is a zone in which nerve cells have become hyperactive. It's thought that a similar pattern of decreased and increased nerve cell activity occurs in the brain of a person with migraine, following the stimulus of a migraine "trigger."
When the activity of nerve cells is depressed, there is impairment of function in the part of the body controlled by these cells. For example, there may be a loss of vision or of strength. Increased activity of brain nerve cells may result in flashing lights or tingling in the face and hand. In the experiments with animals, the depression of nerve cell activity slowly spreads beyond the initial spot of stimulation. This phenomenon is called spreading depression. It is preceded by a wave of increased nerve cell activity.
This slowly spreading depression of nerve cell activity is believed to account for the pattern of development of the typical aura. In the migraine aura, symptoms build up gradually and move slowly from one visual region or one part of the body to another. For example, the migraine aura sufferer may first notice a black spot in the field of vision. This black spot is often surrounded by flashing lights or bright zig-zag lines. The size of the black spot gradually enlarges over a period of minutes. The combination of loss of vision (negative symptoms) with flashing lights or zig-zag lines (positive symptoms) is a typical and distinctive feature of migraine aura. The negative symptom (blacking out of vision) is due to depressed nerve activity; the positive visual symptoms are due to the zone of hyperactive nerve cells. In contrast, a sudden shutting off of blood supply to the brain (as might occur with a blood clot) causes a sudden loss of function. In this case, there is no gradual "march" of visual symptoms or numbness, and positive visual symptoms do not occur.
What starts this sequence of events that leads to the aura and headache? The answers to that question are not fully understood. We do know that migraine sufferers have an inborn susceptibility to factors that normally do not trigger headaches. In people with migraine, changes in body chemistry, such as menstruation, certain foods, and dozens of environmental influences, such as a change in weather, may trigger an attack.
These internal or external events stimulate different nerves of the brain, and these nerves relay the stimuli to one or more nerve centers in the brain stem, the lower portion of the brain that connects with the spinal cord. From these brain stem centers, another set of nerve impulses are sent to the cortex of the brain, causing the aura. The sequence of biochemical events that results in the headache may also begin in these brain stem centers. (See related article, Brain and Migraine.)
(Seymour Solomon, M.D., Headache Unit, Montefiore Medical Center, New York, NY)
Headache, vol. 6, issue 4, December 1995.
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Reprinted from the web site of
the American
Council for Headache Education
(www.achenet.org)
