|Nailing a Migraine:
Hitting It Hard and Early
Gary E Cordingley, MD, PhD
It's bad enough for migraine victims when their heads hurt. But
when a migraine attack reaches a stage when it hurts to even
touch the skin, then that spells double-trouble.
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
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