Heart and Head Misfire Together
By Sam Kean
ScienceNOW Daily News
16 October 2009

Two medical problems caused by misfiring electrical signals, epilepsy
and heart
arrhythmia, probably have a common molecular cause, scientists report.
The
research points to treatments that could lower the chances of young
people dying
of seizures.
The scientists, at Baylor College of Medicine in Houston, Texas, were
studying
mice that had a mutation in the KCNQ gene, which builds potassium ion
channels
that set up an action potential across a cell membrane. These channels
help the
heart beat by resetting the potential after cardiac muscle cells
contract. The
mutation--also found in humans--produces a faulty protein that delays
restoration of the potential, causing erratic beating and sometimes
death.

The ion channel was long thought to operate only in heart muscle, but
recent
work implied that it functions in other tissues. Now Alica Goldman, a
neurologist and co-author of the paper, has discovered the first
definitive
evidence that the channel was working in mouse neurons. It was
especially active
in regions of the brain susceptible to seizures, the researchers
report online
this week in Science Translational Medicine. The team also monitored
the mutant
mice with EEG and ECG machines and determined that seizures often
accompanied
abnormal heart rhythm. "This is exciting because it provides the first
molecular
clue" that potassium ion channels underlie epilepsy and arrhythmia,
says Jeffrey
Noebels, a neurologist and lead author of the paper.

Noebels says misfiring by cells in the brain or heart might spur the
release of
stress hormones that cause the other organ to falter. Or aberrant
electrical
activity in one organ might spread to the other via nerves that
connect them.
But nailing down the exact connections will likely prove tricky. In
the mice,
the relationship between seizures and arrhythmia was erratic: One
frequently
happened without the other.

"The connection is still uncoupled in a sense," says Michael Ackerman,
a
pediatric cardiologist at the Mayo Clinic in Rochester, Minnesota.
Ackerman has
studied severe epilepsy and ion channels, and he says the paper is
primarily a
steppingstone. "The real proof is to go back from mouse to man," he
says. That
means determining how frequently mutations in the KCNQ gene cause
epilepsy in
humans.

Nevertheless, Noebels says the work already points to possible
treatments for
the most serious cases of epilepsy--the 10% of patients, most in their
20s and
30s, liable to die suddenly from seizures. Earlier research in humans
implicated
heart failure in many seizure deaths (Science, 4 July 2008, p. 31).
Noebels
hopes that treatments for faulty potassium channels in cardiac muscle,
such as
beta-blockers and pacemakers, can, if not prevent seizures, at least
prevent
deaths from seizures. "This is the first time we can say, well, if you
have
epilepsy, we should look at your heart, too," he says. "And you don't
have to
wait years to translate this into treatment."

Source: Science
http://sciencenow.sciencemag.org/cgi/content/full/2009/1016/1?etoc