Nailing a Migraine: Hitting It Hard and Early
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