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Les: Since my DBSs in 2003 I've stopped taking the one chlorazapate tablet I used to take every night to sleep. I never have had great sleep habits, but it really is not bad like some attest to. My ocular migraines also stopped after DBS, so I think my brain likes those wires and electric jolts. Ray Rayilyn Brown Board Member AZNPF Arizona Chapter National Parkinson's Foundation [log in to unmask] ----- Original Message ----- From: "Les Combs" <[log in to unmask]> To: <[log in to unmask]> Sent: Tuesday, December 25, 2007 9:47 AM Subject: Re: Sleep Chemical Central To Effectiveness Of Deep Brain Stimulation 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" <[log in to unmask]> To: <[log in to unmask]> Sent: Tuesday, December 25, 2007 2:21 AM Subject: Sleep Chemical Central To Effectiveness Of Deep Brain Stimulation > ScienceDaily (Dec. 24, 2007) — 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. > > ---------------------------------------------------------------------- > To sign-off Parkinsn send a message to: > mailto:[log in to unmask] > In the body of the message put: signoff parkinsn > ---------------------------------------------------------------------- To sign-off Parkinsn send a message to: mailto:[log in to unmask] In the body of the message put: signoff parkinsn ---------------------------------------------------------------------- To sign-off Parkinsn send a message to: mailto:[log in to unmask] In the body of the message put: signoff parkinsn