Re: Norepinephrine and Parkinson's

[Guest guest]

I know that norepinephrine is horrible and shouldn't be used, and doesn't need to be used, except dentists are too lazy to use the alternatives because they don't last nearly as long, which means they have to stay on top and manage the numbing more carefully. You must insist that your dentist use something other than norepinephrine, especially if you know you have any coagulation issues. Norepinephrine stops blood flow to the bone and lack of blood flow results in bone death (necrosis). Looking back, I now realize I had a confluence of events that occured at the onset of my illness. I was repeatedly getting norepinephrine shots in my jaw, because my dentist couldn't get my crowns to fit correctly. Right around that same time, I contracted some kind of untreatable infection at my local YMCA pool that manifested in both my sinuses and in a cut

on I got on my foot at the pool. That's when the migraines started and now years later I realize it was also when one of my crowned teeth became chronically infected. The sad thing is, I probably didn't even need crowns. I just trusted a greedy dentist. This is why I get so ticked off when people say it's my immune system that's letting me down. No, it was really shi**y medical practices that made me sucsceptible enough to get me where I am today with a chronically infected jaw and sinuses. penny a Carnes <pj7@...> wrote: Perhaps on an aside, does anyone see any connection with the fact that many cfs/Lyme patients have trouble with dental ansesthesia and the information in this article? See article below on norepinephrine in dental work. a Carnes August 14, 2007 Fingering the Neural Perp in Parkinson's New study finds its not just dopamine-producing cells, but likely ones that secrete norepinephrine, as well, that kick-start the movement disorder Neuroscientists have long believed that the tremors, stiffness and sluggish gait characteristic of Parkinson's disease resulted from the death

of neurons in a section of the midbrain that produce the neurotransmitter dopamine, which helps to maintain proper motion control. A new study in mice, however, suggests that the disorder may actually be caused not only by hobbled dopamine-producing cells but also by neurons in the locus coeruleus region of the brain stem that produce norepinephrine, a chemical related to dopamine and associated with everything from anxiety to attention to blood pressure regulation. The

new finding could lead to new therapies for combating the debilitating condition. Researchers previously believed that Parkinson's, which affects an estimated 500,000 Americans, most over 60, was triggered when 80 percent of the dopamine-producing neurons in the substantia nigra region of the midbrain died, disrupting the signaling between that structure and another midbrain region called the striatum, which controls motion. But Weinshenker, an associate professor of human genetics at Emory University in Atlanta and senior author of the study published in Proceedings of the National

Academy of Sciences USA, says autopsies on Parkinson's-ravaged brains showed a concurrent loss of norepinephrine-producing cells as well. "The death of norepinephrine neurons has been known among neuropathologists for decades," he says, yet the cells had not been linked to the causation of Parkinson's symptoms. In mouse models of Parkinson's, middle-aged mice (typically one year old) are given a drug called MPTP (or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) that selectively kills their dopaminergic nerve cells. As a result, these mice show much of the same biochemical changes as humans suffering from Parkinson's, but do not display any of the motion problems. "We thought there must be a compensatory system out there somewhere that's kicking in," Weinshenker notes. Weinshenker's team hypothesized that knocking out both norepinephrine-producing and dopamine-manufacturing cells would yield a model closer to the human illness that mimicked Parkinson's-like symptoms. They created a strain of genetically altered animals that could not produce the enzyme dopamine â-hydroxylase, the protein that converts dopamine into norepinephrine. Thus, these animals could produce dopamine, but could not make norepinephrine. The plan was then to selectively kill dopaminergic neurons with MPTP when the mice matured, effectively simulating Parkinson's. But before they had a chance to dampen dopamine function, Weinshenker says, "to our surprise what we saw were Parkinsonian motor deficits." His team ran the animals through a battery of tests to analyze their gait, including their ability to walk a narrowing balance beam, descend a pole and run on a treadmill. "They were impaired on every single test on our battery," Weinshenker notes, adding that some mice developed the hunched posture and tremors that human Parkinson's patients display. "A loss of 80 percent of their dopamine neurons is not enough to cause motor deficit, but loss of norepinephrine is." Weinshenker says that the norepinephrine neurons actually modulate the dopamine release of the substantia nigra neurons. Without norepinephrine, dopaminergic cells can produce the neurotransmitter, but cannot release it—creating the Parkinsonian symptoms. When 80 percent of the dopamine cells are eradicated in mice, however, the brainstem cells can take over and instruct those remaining midbrain cells to make and release more of the motion-controlling chemical. Anesth Prog. 1992;39(3):87-9. Links Adverse reactions associated with norepinephrine in dental local anesthesia. van der Bijl P, Victor AM. Department of Oral Medicine and Periodontics, Faculty of Dentistry, University of Stellenbosch, Tygerberg, South Africa. Two cases are presented in which a 40-yr-old woman and a 20-yr-old woman developed severe headaches after

injection of the local anesthetic Xylestesin-F (3% lidocaine with 1:25,000 norepinephrine). It is suggested that these severe headaches may have been associated with acute transient hypertensive episodes following injection of the local anesthetic. A review of the literature indicates that norepinephrine, at least at a concentration of 1:25,000, should be avoided because of its potential for cardiovascular disturbances. PMID: 1308379 [PubMed - indexed for MEDLINE]