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This is a multi-part message in MIME format. --------------3A4E587B63A Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit Here are a couple of excerpts from one of the studies I cited earlier. The address is: http://hypnos.m.ehime-u.ac.jp/Congress2/CNC.HTM "pseudo" - fake - parkinson's? hmmm curious - Are the symptoms "pseudo" -fake- also. I suppose you should ask the person who has the symptoms. I think (if I am qualified to do such a thing) that the commonly accepted theory about Parkinson's contains a fundamental flaw - It conflicts with what actually happens. I am saying this because when I read things like the post about Steve Mulligan, and I think of all the things that have happened to me that NONE of the experts that I have consulted have been able to even give a partially rational or reasonable explanation for given the current beliefs about PD, it just aggravates me that we determinedly cling to such beliefs when they are contradicted almost daily in practical experience. And yet you can bring up something that is supported and substantiated in real life experiences and they are summarily dismissed with "it's all in your head", or some such non-answer. When some of the contradictory experiences that I have had occurred and I went to my neurologist (who is a movement disorder specialist and VERY KNOWLEDGABLE) for an explanation, I had barely got inside his office and had not yet uttered a word, when he said, "I KNOW what you are going to ask me and I DO NOT KNOW the answer." CHALLENGE your beliefs. CHALLENGE the widely held beliefs. Don't accept PSEUDO answers. And I think you will have to admit that my circumstances were pretty rare - How common is pregnancy w/Parkinson's?and of those how many went off all medications for any length of time at my stage of the disease? The question that naturally first comes to mind when I think I may have stumbled upon (or was mercifully allowed to find out) something not already known, "...AND WHO-O-O do you think YOU are?" And I must always truthfully answer well, uh, NOBODY special", even though I am not unusual, my circumstances certainly were, and maybe that could be the reason. If I would have continued to deteriorate at the same rate I was I don't think I would be alive and if I was I would be in a pitiful state, I was ALREADY to the place I didn't think I could stand anymore of it. The agitation, confusion, pain & etc were about more than I could bear. One day in my frustration that I KNEW I was Emergency Room material, and yet no one could or would DO anything and the PAIN was awful, I finally thought surely I can move SOMEONE, SOMEHOW, so I finally said, "Get me the sharpest thing you can find, if NOBODY will do ANYTHING maybe if I just cut my hands off the pain will be less!" IT WAS SO FRUSTRATING! AND THE ONLY RESULT I GOT FROM THAT WAS THAT I WAS REPRIMANDED FOR UPSETTING THE FAMILY. NOTHING was said about the pain. Now I am leading a quasi-normal life. It's entirely bearable, and sometimes GOOD, and I have HOPE, and it is based on actual happenings, and if NOBODY in the world EVER believes me, (and I think they will) I'm saying it ANYWAY, in hopes for others who are now in the place I was or worse. NO APOLOGIES. To each of you I wish a CHRONIC incurable case of PARIDOXICAL KINESIAS. Thanks, Janet. --------------3A4E587B63A Content-Type: text/html; charset=us-ascii; name="HIST.HTM" Content-Transfer-Encoding: 7bit Content-Disposition: inline; filename="HIST.HTM" Content-Base: "file:///C|/JANET/HIST.HTM" <Bass HREF="file:///C|/JANET/HIST.HTM"> <TITLE>Introduction</TITLE> <P> <H1>Introduction</H1> <P> Histamine (HA) has neurotransmitter roles in the mammalian brain, regulating arousal level and memory retention by stimulating specific receptors on target cells. We have reported that the concentration of HA in the striatum increases after the induction of middle cerebral artery occlusion due to the facilitation in neuronal HA release, and that the inhibition of the activity of histaminergic neurons aggravates delayed damage to hippocampal CA1 pyramidal cells. These findings suggest that the elevated activity of the histaminergic system during ischemia appears to contribute to the neuronal protection. Since excess release of excitatory amino acids such as aspartate and glutamate causes cell death by depolarizing postsynaptic neurons, we investigated the role of the histaminergic system on transmitter amino acids in normal and ischemic conditions.<P> Abbreviation used: HA, histamine --------------3A4E587B63A Content-Type: text/html; charset=us-ascii; name="HIST2.HTM" Content-Transfer-Encoding: 7bit Content-Disposition: inline; filename="HIST2.HTM" Content-Base: "file:///C|/JANET/HIST2.HTM" <Bass HREF="file:///C|/JANET/HIST2.HTM"> <TITLE>Conclusion</TITLE> <P> <H1>Conclusions</H1> <P> <OL> <LI>In normal condition, perfusion of 10 mM HA reduced transmitter amino acids to about 60% or less. This action of HA was antagonized by 1 mM mepyramine, an H1-antagonist, but not by 15 mM cimetidine, an H2-antagonist. A further increase in these amino acids was observed after administration of 10 mM mepyramine. <LI>In ischemic condition, perfusion of 10 mM HA resulted in reduction of the ischemia-induced rise in amino acids to about 50%. These effects of HA were antagonized by 9 mM mepyramine or 15 mM cimetidine. In contrast to the normal condition, cimetidine produced a greater increase in amino acids than in the control group. <LI>These findings suggest that transmitter amino acids were regulated through H1-receptors in normal conditions, but that their rise provoked by ischemia was regulated mainly by H2-receptors. </OL> --------------3A4E587B63A--