vagus nerve compression in CCSVI in MS

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Wed Dec 19, 2012 4:45 pm

1eye wrote:Maybe some things affected by autonomic nerve pathology get more automatic, and some less. Then wouldn't it depend on individual physiological differences, and how they affect specific nerves? And be predictable, but only in a particular individual?

Not only genetic makeup, but life history as well?


That's a big clue...the differences in the disease in all of us. It doesn't mean MS is caused by something different in different people. It means what causes MS is variable in everyone depending on genetics, diet, physiology, stress, etc.

1eye wrote:Does the vagus predominate in the symptoms? Is it involved in intention tremor, which was among my earliest symptoms? Where do eyeballs fit in? Vision is pretty voluntary, so not placebo. In fact, aren't most eyesight improvements very testable, outside of placebo concerns? You can't turn it off without blinking.


The only way to really find out is to organize a study of VNS in PwMS. Anyone know how to throw that together? I'd volunteer for that before I would CCSVI angioplasty. (Unfortunately or fortunately my symptoms probably aren't strong enough to be impressive in a study) Incidentally, I don't think the vagus nerve necessarily has to be directly responsible for tremors, vision, etc issues. Stimulation of the nerve could result in a chain reaction that causes improvement in those issues.

I was reading through CCSVI treatment improvement stories yesterday and saw one instance in which a man went in for his followup checkup and thought he would be given the thumbs up since all of his improvements from treatment were still there. He had restenosed and had to be re-ballooned. To me, this suggests that improvements aren't necessarily dependent upon the ballooning/stenting. What if stimulation of the vagus nerve does correct the hpa axis dysregulation and it is that correction that causes improvements? Aldo has a 35 minute lifespan in our bodies. All that excess aldo could be gone within 35 minutes of VNS and if hyper-response was corrected, it wouldn't build back up. If my theory is correct, this would lead to instant improvement from the reduction of vasoconstrictor aldo and continued improvement as the veins are allowed to heal from all of the damage excess aldo does to them.

Also, as MS progresses, hpa axis dysregulation increases. It seems that the people who opt to have CCSVI have progressed far enough in their disease to take the risk of angioplasty. The correction of a great dysregulation would probably produce startling results.
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Re: vagus nerve compression in CCSVI in MS

Postby Cece » Wed Dec 19, 2012 6:32 pm

1eye wrote:I thought the autonomic nervous system was just that: autonomous, and so by definition not placebo.

I was trying to figure whether or not that was true and I ended up coming to the opposite conclusion: the autonomic nervous system can be affected consciously or subconsciously, and thus can be susceptible to placebo.
It is a well established fact that the autonomic nervous system (ANS) can be influenced by the person and therefore in conjunction with a placebo (i.e., inactive) treatment (Ross & Buckalew, 1985). For example, Cowan, Kogan, Burr, Hendershot, and Buchanan (1990) found that cardiac patients could cognitively increase their HRV through biofeedback training. If the ANS is altered, this result will be shown in HRV measurements.

https://sites.google.com/site/debunking ... ity-claims
HRV is the measurement Dr. Arata is using before and after CCSVI treatment.
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Re: vagus nerve compression in CCSVI in MS

Postby Cece » Wed Dec 19, 2012 6:44 pm

Anonymoose wrote:I was reading through CCSVI treatment improvement stories yesterday and saw one instance in which a man went in for his followup checkup and thought he would be given the thumbs up since all of his improvements from treatment were still there. He had restenosed and had to be re-ballooned.

Surprising, isn't it! Another possible explanation could be that his brain had benefitted from x months of proper blood flow and so the improvements weren't lost when the restenosis occurred. I've heard a few other people say that even though a vein later clotted, the cogfog improvements or vision improvements remained for them; I've also heard people who lost their improvements and then learned they'd restenosed. Another possibility is that these are anecdotes and we can't make too much of one anecdote among thousands. Another possibility is that even with some restenosis, the man's blood flow was still improved from where had had started; my left jugular, for example, was 99% closed, and then treated, and then upon re-examination five months later, it was 60% closed or so. It was improved from where I had before the first treatment but not as good as it was after retreatment.

By CCSVI improvement stories, have you seen the improvement reports thread? I enjoy keeping it up and hope that it can be useful. Everything was linked to a news article so while it was still biased selection (the journalist chose whose story to feature) and anecdotal, it is fairly verified that these people had the treatment and here is what they told the journalists. And it's real names, not internet names like "Cece" and "1eye" who could be shady characters. :) :)
chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic16157.html

not sure if this has been posted before, but it says that the autonomic nervous system is frequently dysfunctional in MS, and related to progression in MS http://www.ncbi.nlm.nih.gov/pubmed/11724449
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Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Wed Dec 19, 2012 7:19 pm

Yes, I've read much of that thread. That is where I picked up on that guy. His continued improvement could be because of months of increased blood flow but does improved blood flow fully account for the immediate improvements? Also, if the vagus nerve is involved maybe that is part of why some people do better than others. Maybe some vagus nerves go untouched. Maybe some are injured. Too many variables!

I had posted a link about the hpa axis dysregulation (autonomic) that increased with progression of ms in my original Aldo thread. The question is...which came first? The dysregulation or the ms? Is dysregulation driving the ms? That would account for the variability in the way ms presents and progresses in different people.
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Re: vagus nerve compression in CCSVI in MS

Postby Cece » Wed Dec 19, 2012 7:23 pm

Anonymoose wrote:I had posted a link about the hpa axis dysregulation (autonomic) that increased with progression of ms in my original Aldo thread. The question is...which came first? The dysregulation or the ms? Is dysregulation driving the ms? That would account for the variability in the way ms presents and progresses in different people.

It could be entangled too. Worsening MS worsens the dysregulation, and the dysregulation worsens the MS.
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Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Wed Dec 19, 2012 7:49 pm

I'm trying to put this down for the night but my mind keeps whirling.

It seems like if stimulating the vagus nerve results in instant correction of the hpa axis dysregulation, the dysregulation is not the result of any degeneration/ms activity. More likely it is the result of chronic elevated expression of cortisol, Aldo, etc resulting in reduced sensitivity which winds up causing the body to produce more trying to spur the original level of response...like a drug addict who needs more to get same high. Seems like reduced sensitivity must be an issue or we would all be living in the cardiac ward.

How stimulating the vagus nerve would inspire such a correction is beyond me. Very odd.

Edited to add: it won't stop whirling! Maybe touching the vagus sends a shock wave out to hpas?

Second edit: I think they can correct some heart rhythm issues by stopping and starting the heart. Then there are pacemakers resetting natural rhythms. Could glands act this way too? Reset by shock?
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Re: vagus nerve compression in CCSVI in MS

Postby 1eye » Wed Dec 19, 2012 9:22 pm

I would believe you if you told me shock would affect the heart rhythm. Though I didn't know what you meant by shock. Going into shock surely affected mine. Incidentally I blame the epinephrine most dentists include with novocaine. My heart has not bothered me at the dentist's since I forbid them to use epinephrine on me.
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Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Thu Dec 20, 2012 9:38 am

I was thinking shock in the sense that maybe touching the nerve sends an unexpected signal to the hpa's causing them to reset. I was wrong. :P Btw, you earned at least 20 macho man points for divulging that you have your dentistry done w/o novocaine. Or do they have novocaine w/o epinephrine in it?
Odd vagal connection w/epinephrine that I haven't considered much or explored...
http://www.apa.org/monitor/apr04/vagus.aspx
This experiment supported the researchers' first hypothesis, that vagal nerve stimulation produces dramatic surges in norepinephrine in a brain area involved with memory storage, a finding that almost certainly generalizes to humans. What's more, Williams says, "The magnitude and time course of changes in amygdala norepinephrine almost mirrored the changes produced by the dose of epinephrine that has been shown to improve memory."

Anyway...a start towards understanding how VNS might correct hpa axis dysregulation...
(cortisol is made in the fasciculata which is directly connected with zona glomerulosa which produces aldosterone)
http://www.ncbi.nlm.nih.gov/pubmed/3659545
Vagal influence on the adrenocortical function of the rat.
González-Fernández I, Gonzalo-Sanz LM.
Source
Departamento de Anatomía, Facultad de Medicina, Universidad de Navarra, Pamplona, Spain.
Abstract

The vagal influence on the fasciculata's function was studied in 23 Wistar male rats. The corticoadrenal function was evaluated by means of karyometric and histological studies. After vagotomy, the fasciculata of the left adrenal (operated side) showed a significant increase of the nuclear area in comparison with the right (control) side. This side difference was maintained in the stressed rats. In these animals the nuclear area did not increase significantly in either of the two adrenals. These results lead to the following conclusions: the vagus nerve, in normal conditions, has an inhibitory influence on the adrenal cortex; the vagal participation in the corticoadrenal response to a neurogenic stressor is meagre; the inhibitory vagal action on the fasciculata must be direct since the corticoadrenal modifications were unilateral, whereas, if the vagal influence were exerted through the hypophysis, the adrenal reaction should be bilateral; and, finally, the participation of the vagus nerve in the adrenal vascular disorders, which appeared in the stressed rats, seems to be insignificant since both glands, vagotomized and non vagotomized, showed a similar appearance.
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Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Thu Dec 20, 2012 12:09 pm

This is getting messy...
First, you can stimulate the vagus nerve through maneuvers and massage...so CCSVI angioplasty very well may cause VN function changes.

This study shows the opposite response to stimulation compared to depression study previously linked...don't know what to think about that...maybe the difference is that subjects didn't already have hpa axis dysregulation?
http://ajpregu.physiology.org/content/279/1/R141.short
Electrical stimulation of afferent vagus nerve induces IL-1β expression in the brain and activates HPA axis

And possible alteration in immune response due to VNS...
http://www.brainimmune.com/index.php?op ... Itemid=420
Role of the Vagus Nerve at the Neural-Immune Interface
Image
Afferent vagal pathways transmit information to the brain related to peripheral inflammation so as to participate in the activation of adaptive reactions, including fever and sickness behavior. On the other side, efferent vagal pathways inhibit the synthesis and release of pro-inflammatory cytokines by peripheral immune cells. Because activation of afferent vagal pathways by immune stimuli leads to suppression of immune reactions, the term inflammatory reflex was introduced. The inflammatory reflex adjusts the intensity and duration of inflammatory reactions according to actual needs, thus protecting an organism from tissue damage induced by excessive inflammation. Both experimental and clinical studies suggest that inappropriate activation of the inflammatory reflex participates in the development of diseases characterized by excessive production of cytokines.', '
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Re: vagus nerve compression in CCSVI in MS

Postby Cece » Thu Dec 20, 2012 12:21 pm

But this is talking about effects of vagus nerve stimulation, and that is an implanted device that stimulates the vagus nerve repeatedly over the course of the day, for months on end? Have vagus nerve stimulation devices ever been tried in MS? Over at the Mousedoc blog, one of the neurologists made the statement that autonomic nervous system dysfunction is rare in MS. I looked into if there is research showing this one way or another. There is some research supporting autonomic nervous system dysfunction in MS, but there is a paucity of research one way or another. It is possible that autonomic dysfunction leads to impaired thermoregulation, which leads to difficulty of the body cooling itself, which leads to strain on neurons that are functioning at their absolute limits and beyond, which contributes to Wallerian degeneration and excessive neural apoptosis. For all the money spent on MS research every year, this is yet another unexplored aspect.

Instead of looking at vagus nerve stimulation, is there any research on what symptoms occur when a vagal nerve is continuously compressed such as by a jugular with stasis of flow? Or what symptoms are relived when the compression is corrected.

Keep the thoughts whirling, Anonymoose. And did I read that you are trying out a drug that affects aldosterone? Keep us informed, please, with how that goes.

LOL, I don't have to say keep the thoughts whirling, there is a new post while I was composing this.
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Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Thu Dec 20, 2012 12:28 pm

LOL! Temporary stupification of whirling thoughts as I say to myself "what the heck is she talking about?!" Wallerian? Really? You do dazzle me! :D

I will be starting eplerenone early to mid January. Of course I'll keep you all up to date on my obsession. Like you could shut me up. :P

I have to stop obsessing for now. Must. Pay. Bills. Bleh.
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Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Thu Dec 20, 2012 12:46 pm

One more thought...

Maybe it is the compression (massage?) of the vagus nerve by the jugular that causes hyperstimulation of hpa axis in some cases.

Okay...now bills. I hope.

Nope...not bills.

Maybe the compression initially sets off the hpa axis dysregulation but the tendency of that dysregulation to lead to further dysregulation leads to progression of MS. The vagus wouldn't have to be compressed any more or any differently in order for the hpa axis to go completely haywire.

Oh and I read somewhere that vagus issues can lead to b12 absorption issues.

Now bills or I risk losing internet access.
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Re: vagus nerve compression in CCSVI in MS

Postby 1eye » Thu Dec 20, 2012 1:13 pm

Thermometer being out of control is a very reliable symptom for me.

Stress causes the release of adrenaline. With me, more than about half a day of continuous high stress with simultaneous adrenaline (+cortisol, +aldo? +?) release has been enough to trigger an unexpected near-blindness "MS" incident. Not sure if this was due to the length of the fall, or the sudden stop at the end (so to speak). Vision was improved by pulse of cortisone.

The reaction to heat is so generalized, I think it must be brain-heat, although neck cooling helps me a lot.

Another aside: yes they have, but don't advertise, novocaine without epinephrine. The adrenaline makes you bleed less, which is why they like using it. It's a Darwinian stress reaction -- constriction of blood vessels (veins too?) by the smooth muscle layer so that cuts are less of an immediate threat.

I am intrigued by smooth muscle control of vessel diameter. It has a powerful, fourth-power effect on vessel resistance to flow, so I would think it affects whether and how much blood flow remains laminar, and that the more the vessels are constricted, the harder your heart has to work to get the oxygen circulating. So it beats faster. Incidentally, other things being equal, the more vessels are constricted, the less effective they are at cooling. Not so important when threats loom.
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Re: vagus nerve compression in CCSVI in MS

Postby PointsNorth » Thu Dec 20, 2012 3:33 pm

@moose Can I ask where you read about the vagus-b12 connection? I am really struggling with B12 malabsorption issues. My IBD became out of control at the time B12 absorption became an issue. Vagus also connected with bowel....

pwMS are apparently B12-deficient and this would lead to elevated homocystiene levels in some. High homocysteine levels can lead to many vascular events (stroke/heart attack) along with venous/arterial thrombosis. Perhaps b12 deficiency is near the top of the "cascade". Please comment :?

Also, earlier on this thread (I think) I posted about a German company offering an external VNS device. I wrote to them but never heard back. I think they are trying to get certification for sale in Europe . . . let me try to find. Voila:

http://www.neurotechreports.com/pages/N ... evice.html

http://us.cyberonics.com/en/


A string of frequencies/vibrations possibly. Maybe 1eye can build us one? Maybe I just need to hold my electric razor behind/below ear? Not far from the atlas v. and the TMJ!?
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Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Thu Dec 20, 2012 6:57 pm

Hi PN,
I couldn't find the page I had read before regarding the vagus nerve and b12. It's funny (and annoying!) how a slight change in search terms can return such different results. There are tons of links about vagotomy and b12 deficiency. This paper offers some clues about what might be happening.

Some background...the vagus nerve plays a big part in gastric parietal cell activity. The parietal cell secretes intrinsic factor which is essential to b12 absorption.

http://informahealthcare.com/doi/abs/10 ... 9109111222
Intrinsic Factor Secretion and Cobalamin Absorption: Physiology and Pathophysiology in the Gastrointestinal Tract

1991, Vol. 26, No. s188 , Pages 1-7
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H. P. M. Festen†
Groot Ziekengasthuis,'s-Hertogenbosch, The Netherlands
†Correspondence: Dr. H.P.M. Festen, Dept. of Internal Medicine, Groot Ziekengasthuis, Nieuwstraat 34, 5211 NL's-Hertogenbosch, The Netherlands

Intrinsic factor is produced by the gastric parietal cell. Its secretion is stimulated via all pathways known to stimulate gastric acid secretion: histamine, gastrin, and acetylcholine. There is, however, a different mode of secretion for both substances: atropine, vagotomy, and H2 receptor antagonists inhibit both intrinsic factor and acid secretion, but secretin and the hydrogen-potassium ATPase antagonist omeprazole have no effect on intrinsic factor while substantially reducing acid secretion. Cobalamin in food is bound to animal protein. Cobalamin deficiency due to inadequate dietary intake is rarely seen in extreme vegetarians (vegans). In the stomach cobalamin is liberated from its protein binding by peptic digestion and bound to R-proteins. Hypochlorhydria or achlorhydria, whether medically induced or not, may impair cobalamin uptake. The cobalamin-R-protein complex is split by pancreatic enzymes in the duodenum, where cobalamin is bound to intrinsic factor. Pancreatic insufficiency may lead to cobalamin deficiency. Lack of intrinsic factor is the commonest cause of cobalamin deficiency; very rarely, aberrant forms of intrinsic factor are produced, but the clinical syndrome is similar. Gram-negative anaerobe bacteria bind the cobalamin-intrinsic factor complex, and bacterial overgrowth of the small intestine diminishes cobalamin resorption. Parasitic infections with fish tapeworm and Giardia lamblia are also associated with cobalamin malabsorption. The cobalamin-intrinsic factor complex binds to the ileal receptors in the terminal ileum. Cobalamin absorption may be impaired after resection or by diseases affecting more than 50cm of the terminal ileum, such as Crohn's disease, coeliac disease, tuberculosis, lymphoma or radiation. There is clearly a wide diversity in the aetiology of cobalamin deficiency, which requires a versatile diagnostic approach.

Read More: http://informahealthcare.com/doi/abs/10 ... 9109111222


The vagotomy and b12 deficiency link makes it seem like holding your electric razor to your head might be a good idea. However, I'd hold off on that for a bit as it seems that there is conflicting info out there about what the vagus nerve may be doing in ms. The depression study hinted that stimulation of the vagus nerve might correct dysregulation. But this paper shows that it may be too much stimulation of the vagus nerve that causes dysregulation.
http://ajpregu.physiology.org/content/279/1/R141.short
Electrical stimulation of afferent vagus nerve induces IL-1β expression in the brain and activates HPA axis

Maybe it's different things in different people but I wouldn't mess around with your vagus until we have a better idea. Do b12 injections work?
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