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Re: Sleep Chemical Central To Effectiveness Of Deep Brain Stimulation


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I have trouble getting more than 5 to6 hours of sleep at night.  Wake up
feeling anxisious.  Sometimes I take a xanax at about 4:30 am to 5:30 am and
sleep another 3 hours or so.  I invariably have reduced symptoms during the
day when I do this.  Could the "sleep chemical" mentioned in the study hae
anything to do with this?  Anyon else out there have similar experiences?

Les


----- Original Message ----- From: "M.Schild" <mmoo@xxxxxxxxxxxxxxxx> To: <PARKINSN@xxxxxxxxxxxxxxxxxxxx> Sent: Tuesday, December 25, 2007 2:21 AM Subject: Sleep Chemical Central To Effectiveness Of Deep Brain Stimulation


ScienceDaily (Dec. 24, 2007) â A brain chemical that makes us sleepy also
appears to play a central role in the success of deep brain stimulation to
ease symptoms in patients with Parkinson's disease and other brain
disorders.
The surprising finding is outlined in a paper published online Dec. 23 in
Nature Medicine.
The work shows that adenosine, a brain chemical most widely known as the
cause
of drowsiness, is central to the effect of deep brain stimulation, or DBS.
The technique is used to treat people affected by Parkinson's disease and
who
have severe tremor, and it's also being tested in people who have severe
depression or obsessive-compulsive disorder.
Patients typically are equipped with a "brain pacemaker," a small
implanted
device that delivers carefully choreographed electrical signals to a very
precise point in the patient's brain. The procedure disrupts abnormal
nerve
signals and alleviates symptoms, but doctors have long debated exactly how
the procedure works.
The new research, by a team of neuroscientists and neurosurgeons at the
University of Rochester Medical Center, gives an unexpected nod to a role
for
adenosine and to cells called astrocytes that were long overlooked by
neuroscientists.
"Certainly the electrical effect of the stimulation on neurons is central
to
the effect of deep brain stimulation," said Maiken Nedergaard, M.D.,
Ph.D.,
the neuroscientist and professor in the Department of Neurosurgery who led
the research team. "But we also found a very important role for adenosine,
which is surprising."
Adenosine in the brain is largely a byproduct of the chemical ATP, the
source
of energy for all our cells. Adenosine levels in the brain normally build
as
the day wears on, and ultimately it plays a huge role in making us
sleepy --
it's the brain's way of telling us that it's been a long day, we've
expended
a lot of energy, and it's time to go to bed.
The scientists say the role of adenosine in deep brain stimulation has not
been realized before. Even though scientists have recognized its ability
to
inhibit brain cell signaling, they did not suspect any role as part of
DBS's
effect of squelching abnormal brain signaling.
"There are at least a dozen theories of what is happening in the brain
when
deep brain stimulation is applied, but the fact is that no one has really
understood the process completely," said Robert Bakos, M.D., a
neurosurgeon
at the University of Rochester and a co-author of the paper, who has
performed more than 100 DBS surgeries in the last decade. "We've all been
focused on what is happening to the nerve cells in the brain, but it may
be
that we've been looking at the wrong cell type."
Nedergaard's team showed that the electrical pulses that are at the heart
of
DBS evoke those other cells -- astrocytes -- in the area immediately
around
the surgery to release ATP, which is then broken into adenosine. The extra
adenosine reduces abnormal signaling among the brain's neurons.
The team also showed that in mice, an infusion of adenosine itself,
without
any deep brain stimulation, reduced abnormal brain signaling. They also
demonstrated that in mice whose adenosine receptors had been blocked, DBS
did
not work; and they showed that a drug like caffeine that blocks adenosine
receptors (the reason why caffeine helps keep us awake) also diminishes
the
effectiveness of DBS.
"It may be possible to enhance the effectiveness of deep brain stimulation
by
taking advantage of the role of agents that modulate the pathways
initiated
by adenosine," said Nedergaard. "Or, it's possible that one could develop
another type of procedure, perhaps using local targeting of adenosine
pathways in a way that does not involve a surgical procedure."
The latest work continues Nedergaard's line of research showing that brain
cells other than neurons play a role in a host of human diseases. ATP in
the
brain is produced mainly by astrocytes, which are much more plentiful in
the
brain than neurons. Astrocytes were long thought of as simple support
cells,
but in recent years, Nedergaard and colleagues have shown that they play
an
important role in a host of diseases, including epilepsy, spinal cord
disease, migraine headaches, and Alzheimer's disease.
The research on DBS came about as a result of a presentation Nedergaard
made
to colleagues about her research on astrocytes. Bakos linked her detailed
description of astrocyte activity to what he sees happening in the brain
when
deep brain stimulation is applied. Based on Bakos' experience in the
operating room and with funding from the National Institute of
Neurological
Disorders and Stroke, Nedergaard went back to the laboratory and analyzed
the
effects of deep brain stimulation in a way that no one had ever before
considered.
"The correlation between what we see in the clinic and Dr. Nedergaard has
found in the laboratory is really quite startling," said Bakos. "All the
credit goes to her and her team. This has been a nice interchange of
information between the clinic and the laboratory, to speed a discovery
that
really could have an impact on patients."
The lead authors on the paper are post-doctoral research associate Lane
Bekar,
Ph.D., and neurosurgeon Witold Libionka, M.D. The Rochester team is based
both in the Department of Neurosurgery and the Center for Translational
Medicine. In addition to Nedergaard and Bakos, other authors from
Rochester
include research assistant professors Guo F. Tian and Takahiro Takano;
graduate students Arnulfo Torres and Ditte Lovatt; technical associate
Qiwu
Xu; former post-doctoral research associate Xiaohai Wang; and Erika
Williams,
a Fairport native and an undergraduate student at Williams College. Jurgen
Schnermann of the National Institutes of Health also contributed.
Adapted from materials provided by University of Rochester Medical Center.

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