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A Diagram/information About The Vagus Nerve/brainstem That Everyone With Pots Should See


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thanks to richgotspots for the motivation :)

The Heart: http://ajplegacy.physiology.org/content/130/4/729.extract (take off the nerves, the heart still beats--really weird, an oldie but a goodie)

Note: CN X= the vagus nerve coming out of the brainstem--SA(Sinoatrial node) is the heart's pacemaker. see below.

The Vagus nerve : http://dc127.4shared.com/doc/RwDmxbNv/preview_html_m1411d1b4.jpg ( a great diagram)

Where the vagus nerve enters the brain: http://12cranialnerves.files.wordpress.com/2012/04/brain_stem.jpg-- medulla oblongata( respiration/breathing, heart, baroreceptors(blood vessel receptors), (vomiting, coughing, sneezing, swallowing)

The reticular activating system (RAS) : (vascular dilation) (sleep-wake cycle) (overstimulation)http://en.wikipedia.org/wiki/Reticular_formation#Anatomy

The Pons: where your thought communicate to your ANS--where your conscious/subconscious thoughts can affect your ANS.

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great article, brain stimulator. This is forward to research worthy. Yeah, piracetem sounds like a very interesting drug...or i guess you could just use coffee grounds :D

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Interesting case study in that it documents a substantial decrease in cerebral perfusion with POTS, yet had an increase in blood pressure.

I don't know why the mayo clinic is maintaining the view that cerebral perfusion is not compromised in POTS patients with studies like these.

Vagal palsy seems like a much more severe form of autonomic disturbance than what most POTS patients present. (The dysphagia + slurred speech for example) so maybe that's representing the extreme of parasympathetic withdrawal.

But then also there have been vagal palsy patients without POTS, so the conundrum still exists.

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Do Mayo still say that? gees. I think even Novak (the guy that published the study saying autoregulation was fine in POTS) suggested that they might have got it wrong. There is now myriad of studies from very different research groups all reporting either autoregulation locked to BP fluctuations or just reductions in cerebral artery velocity.

While some studies used small cohorts, at least in NET deficiency there is evidence of abnormal cerebral autoregulation and this area is being investigated rigourously (yes, i used the word rigourous!)

How the vagas is implicated and in which subsets (or is it a subset of its own) I dont really know but its defintaely worth exploring as there is potential perhaps for enhancing of the central parasympathetic system and I am currently unaware of anyone treating pots with centrally acting acetylcholinesterase inhibitors.

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Do Mayo still say that? gees. I think even Novak (the guy that published the study saying autoregulation was fine in POTS) suggested that they might have got it wrong. There is now myriad of studies from very different research groups all reporting either autoregulation locked to BP fluctuations or just reductions in cerebral artery velocity.

While some studies used small cohorts, at least in NET deficiency there is evidence of abnormal cerebral autoregulation and this area is being investigated rigourously (yes, i used the word rigourous!)

How the vagas is implicated and in which subsets (or is it a subset of its own) I dont really know but its defintaely worth exploring as there is potential perhaps for enhancing of the central parasympathetic system and I am currently unaware of anyone treating pots with centrally acting acetylcholinesterase inhibitors.

Yes, Novak might have been wrong, but the data is still there, unless he messed up collecting the data, which I doubt somewhat. Additionally, even Stewart's study didn't really demonstrate appreciable significance between controls and POTS CBF. I think controls reduced by 12% and POTS by 19%

however, in astronauts before space flight they did TTT on them and found their CBF decreased by 28%. These are astronauts before space flight without POTS.

http://jp.physoc.org/content/579/3/799.full.pdf

So that 19% or so reduction found by Stewart's group doesn't really concern me.

Now, the POTS patient cited in this study does concern me, as that's >50% in cerebral blood flow, nearing almost ischemic levels. That most certainly is a very dangerous level of blood flow.

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Unpublished data from the Baker Institute suggested a reduction of arouund 40% with cerebral vasospasm.

Most of the studies of cerebral bloodflow in POTS have found cerebral autoregulation buffering of beat by beat blood pressure changes is abnormal and cerebral blood flow velocity changes intermittently with blood pressure. So rather than the reduction in overall blood brain perfusion these studies are suggesting that cerebral autoregulation is basically failing completely.

http://europace.oxfordjournals.org/content/4/4/369.full.pdf

http://europace.oxfordjournals.org/content/8/3/199

50% is quite scary and interesting.

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Unpublished data from the Baker Institute suggested a reduction of arouund 40% with cerebral vasospasm.

Most of the studies of cerebral bloodflow in POTS have found cerebral autoregulation buffering of beat by beat blood pressure changes is abnormal and cerebral blood flow velocity changes intermittently with blood pressure. So rather than the reduction in overall blood brain perfusion these studies are suggesting that cerebral autoregulation is basically failing completely.

http://europace.oxfordjournals.org/content/4/4/369.full.pdf

http://europace.oxfordjournals.org/content/8/3/199

50% is quite scary and interesting.

The abnormal oscillatory pattern of CBVF in POTS is a recurring theme that Stewart reproduced, In the first study you cited, CBF was generally maintained ~20% reduction for most of the TTT until syncope occurred. One thing that bothers me is the lack of reproducible data. Between Schondorf, Stewart, Hermosillo, and Jacob, they're all getting quite different results, except for Stewart and Jacob, who're roughly close to each other with ~20% reduction cited.

I'd be interested to see the Baker Institute's results, especially if they had a larger study as I think a larger cohort is required to flush out the differences.

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Lemon- you're welcome :)

Jangle- back when I had my first Pots theory it related to various regional perfusion issues. I suggested that they use a very simple TTT brain SPECT test that could easily these issues. I know Cleveland now uses some nuclear testing for perfusion but Idk if it has lead to any real treatments. When BP issues are isolated to lungs for example, systemic BP can be totally different. I believe that has also been seen with Kidney BP as well. Systemic BP meds affect the region areas just not profoundly enough and then they can alter the systemic BP too much in the wrong direction..

I have found links between NOS and small fiber neuropathy. Loose connective tissue surrounds surround blood vessels and nerves. It also attaches epithelial tissue to organs. Epithelial tissue is responsible to NO regulation and some how the damaged nerves messing with epithelial's regulation. Its like a reffered short circuit or dysfunction..

Rama- thanks for the study, good to see some international work like this.

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Also keep in mind in these studies testing the cerebral blood flow decline they're being done on the TTT, which takes away the skeletal muscle pump. Even normal people will faint eventually without their skeletal muscle pump. In actual standing even someone with POTS will have their skeletal muscle pump greatly assisting their CBF, so you won't get the more exaggerated 40% reductions seen on the TTT. Additionally, those large of reductions are occuring with longer TTT durations, and for patients who have syncope (which would obviously drop the maximal CBFV) however, the majority of POTS patients don't have syncope. So some of the variation between the studies can be explained by the study population they use, maybe one uses POTS patients who have syncope and the others don't. Additionally maybe some have longer TTT durations than others.

As I cited, the (we assume normal) astronauts pre-flight had a cerebral blood flow velocity decrease of 25% after 10 minutes. It was continuing to decrease from the 5-10 minute mark, so it could probably be deduced if they held them up the 16-20+ minutes other studies are showing you would see an even greater decrease than 25%, maybe even reaching into the mid-30's and 40's that the POTS papers are showing.

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So you believe that the reductions in cerebral blood flow in pots are no different to normal people?

in low flow pots it appeared that the skeletal muscle pump was fAulty but ignoring that point for a moment in pots there are consistent findings of reduced stroke volume. Even if orthostatic cerebral autiregulation is maintained it would fail eventually without adequate cerebral blood supply but a cardinal symptom of pots is symptoms of cerebral hypoperfusion without reductions in overall blood pressure.

so I'm curious how you explain that if you believe cerebral blood flow is normal in pots.

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When I had my tilt table test my carotid artery blood flow was monitored and was found to decrease by around 35% at that time which was then inferred to be the result of cerebral vasospasm.

Dr Stewart found that rather than auto regulatory deficits, some pots don't have cerebral venous vasodilation in response to cognitive challenge.

finally recent work by grubb's group looked at hypertensive and normotensive syncope where cerebral vasoconstriction dominate but where blood flow is not reduced, o the left side of the auto regulatory curve has been pushed too far right as an adaption to hypertension thus fails at normal but lower Bp values.

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I do believe blood flow is being reduced, but I think for the majority of POTS patients without syncope the difference between normal and POTS is not as a large as some of the studies suggest. Stewart's paper of about a 8 or so % difference seems about right given the data I've seen. Also keep in mind Schondorf's study of a rather large group of POTS patients ~30, did not show any difference in CBF or autoregulation between POTS and controls. This can't be ignored, and in the studies demonstrating larger reductions >20% or so, one has to question if this is really outside of normal. As the astronaut study I cited demonstrates normal people can have >25% reduction after 10 minutes, it calls into question some of these studies with the higher numbers as they did not use controls and the study population they used may be on the more extreme end of POTS of those patients presenting with syncope.

My own personal view again is somewhere in the middle, which is where Stewart's paper resides I believe. As he did use controls, it's more scientifically valid, but on the other hand, Schondorf also used controls and found the negative result. POTS is mysterious, and the physiology involved is very complex. The symptoms of hypoperfusion could be the result of advanced messages to the brain of impending autoregulatory failure rather than from actual autoregulatory failure, or it could be from the oscillatory pattern Stewart demonstrated i.e. the 5 seconds of high CBFV, matched with the 5 seconds of reduced cerebral blood flow - and the symptoms come from the reduced cerebral blood flow period.

Either way, the science is not settled and am I'm not convinced of either direction based off what we currently have. What's needed is a study with a large cohort of a representative population of POTS patients with controls.

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Interesting. It is odd and I remember when I asked one of the doctors about they said they couldnt- at that time - explain why the profound feelings of dizziness from reasonable low overall reductions in cerebral blood flow. I wonder if the vasomotor nerves are compromised or whether increased cerebral vasoconstriction effects blow flow or certain areas of the brain?

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