Most people with migraine attacks learn that they have more success if they treat their attacks early rather than delaying medication until two or more hours have passed. They find there is a window of opportunity during which they can resolve their headaches completely, but if they wait too long, then in most cases the treatment is not nearly as good, and the attacks run their full course.
Particularly observant victims of migraine attacks might also discover that when their migraines get to a stage called "allodynia" when everything hurts--even a light brush to the skin or contact with a warm object--then treatment is likewise less successful.
The chances to make these kinds of observations have been available to people with migraine for as long as there have been decent treatments. Aspirin was the first good, widely available treatment for migraine attacks, and was manufactured in tablet form as long ago as 1915. But it has been in only the last few years that scientific studies have explored these phenomena in detail, and revealed some of the secrets as to why they occur.
Dr. Rami Burstein and colleagues at the Beth Israel Deaconess Medical Center in Boston performed a study of treatment outcomes in a total of 61 migraine attacks occurring in 31 patients. In some attacks treatment was given within the first hour of symptoms, while in other cases treatment was purposely delayed until four hours after the attack's onset. The treatment used was a "triptan" drug, rather than a painkiller. Triptans are a newer group of medications that act on some of the nervous system's receptors for the natural chemical serotonin. In each case, the patient also received a physical examination at the time of treatment to determine whether or not allodynia was present.
What the investigators found was that in the 34 attacks in which allodynia had already developed, the triptan stopped pain within two hours in just 15% of the attacks. But in the 27 attacks in which allodynia had not yet developed, the triptan was successful in 93% of the attacks. While allodynia was more frequently present in attacks that were treated late, the doctors found that the presence or absence of allodynia was more important in determining the success of the treatment than whether or not the treatment was late.
Dr. Burstein also headed a team of scientists that found out why this is the case. Because this information could not be obtained in humans, test tubes or computers, these experiments were performed in laboratory rats. Burstein developed a procedure for simulating migraine attacks in rats and via tiny electrodes he was able to "listen in" on the electrical activity of individual nerve and brain cells as the attacks developed.
What he found was that at the beginning of an attack, nerve cells connecting various membranes within the head to the brain were the first to become overactive in their firing patterns. The excessive activity in these nerve cells, in turn, drove a second set of pain-processing cells located within the brain into their own state of overactivity. If this second group of cells remained hyperactive for too long, then they became "sensitized" and kept firing away, as if on autopilot, even if the nerve cells that got them going in the first place were shut down. In this state of spontaneously self-regenerating overactivity of the pain-processing brain cells, it could be shown that ordinarily non-painful stimuli applied to the skin of the rats were handled by the nervous system as if they were painful. Or, said another way, the development of allodynia in the rat signaled that the pain-processing brain cells had become sensitized.
Just as in the humans, triptan drugs could be administered to the rats at different stages of the migraine attacks. If the triptan was administered before the pain-processing brain cells had become sensitized, then it was able to shut down the cascade of excessively firing cells and stop the attack. But if the triptan was given after sensitization had occurred, then it was ineffective.
Collectively, these studies in humans and rats build a powerful case that what humans need to do in order to be successful in stopping their migraine attacks is to treat them before their pain-processing brain cells have become sensitized. And the best way to tell if sensitization has occurred is according to whether or not ordinarily non-painful contacts to the skin have become painful. In short, migraine patients need to race the clock to treat their attacks before the development of allodynia.
(C) 2005 by Gary Cordingley
