Stomach Pooling In A Variety Of Pots

[ramakentesh]

Im one of the POTS patients that do not exhibit blood pooling in my legs or hands - infact when im symptomatic I usually have obvious and extreme vasoconstriction of my hands and feet, as well as my legs and arms - so peripheral vasoconstrictors are only marginally helpful thus far for me.

I was told originally that this is the result of excess norepinephrine as a response to standing and that was causing wholebody vasoconstriction and my symptoms of POTS.

here is another hypothesis - exclusive stomach pooling possiblty being caused by excess pooling restricted purely to the stomach region in 'Normal Flow POTS'

These patients seem to exhibit severe peripheral vasoconstriction as a counter to this pooling which seems to occur without any autonomic defect:

it is suggested that there could be a local (stomach) inflammatory reaction of some kind that is causing this. As examples, inflmmatory markers like Substance P and Calcitonin gene related peptide are known to cause excessive nitric oxide release in migraine head aches that result in vasodilation. This counters the vasoconstrictive effects of the sympathetic nervous system.

http://ajpheart.physiology.org/cgi/content/full/289/5/H1951

The strange thing is that I also have another inflammatory condition that arrived within months of my POTS - and originally i suffered from severe post-prandial pooling.

[ramakentesh]

And check this out - post prandial smoking reduces post meal abnominal pooling...

http://www.jultrasoundmed.org/cgi/content/abstract/23/5/647

Im not suggesting any one go out and start smoking cubans but its interesting all the same.

[Shimoda]

Certainly interesting...

[bjt22]

Very interesting.

I'm one who pools everywhere....arms, legs, abdomen, etc. However, at the same time, I have patchy vaso-constriction going on in various areas.

For me, it comes down to trying to keep things on as even a keel as possible. This usually means I'm trying to keep those constrictive spasms from occurring. I've not had any luck with the vasodilation. Any attempt to correct it causes vasoconstriction in areas I don't want it. I just have to live with the effects.

I will confess to being a smoker, and I think it does help. As does caffeine. These are very mild vasoconstricters, and when one has used these for a long, long period of time, they don't cause problems. However, I could see how one might encounter problems if one had not used these substances before.

Very interesting about the migraines. I do happen to think that migraine is an autonomic dysfunction in and of itself, but the mechanisms are very unclear. Incidentally, I've described myself as feeling as if I "have an entire body migraine all the time".

[firewatcher]

Im one of the POTS patients that do not exhibit blood pooling in my legs or hands - infact when im symptomatic I usually have obvious and extreme vasoconstriction of my hands and feet, as well as my legs and arms - so peripheral vasoconstrictors are only marginally helpful thus far for me.

I was told originally that this is the result of excess norepinephrine as a response to standing and that was causing wholebody vasoconstriction and my symptoms of POTS.

here is another hypothesis - exclusive stomach pooling possiblty being caused by excess pooling restricted purely to the stomach region in 'Normal Flow POTS'

These patients seem to exhibit severe peripheral vasoconstriction as a counter to this pooling which seems to occur without any autonomic defect:

it is suggested that there could be a local (stomach) inflammatory reaction of some kind that is causing this. As examples, inflmmatory markers like Substance P and Calcitonin gene related peptide are known to cause excessive nitric oxide release in migraine head aches that result in vasodilation. This counters the vasoconstrictive effects of the sympathetic nervous system.

http://ajpheart.physiology.org/cgi/content/full/289/5/H1951

The strange thing is that I also have another inflammatory condition that arrived within months of my POTS - and originally i suffered from severe post-prandial pooling.

Would this suggest that we are getting MIGRAINES as our body's response to our ANS problems as a compensatory mechanism?????????????? I have read that the initial NO dump in migraine genesis is depleted rapidly and that it is excessive dopamine and the other neurotransmitters that actually causes the headache. (? will look for that article again.)

[ramakentesh]

It could be a compensatory mechanism - or it could just be because our sympo systems are over excited? Until they understand migraines properly they might not know.

As for the comment about a whole body migraine - yeah i often feel exactly the same! Things that trigger migraines in people wiht migraines tend to trigger POTS symptoms in me. I also read of a small group of migraine patients have POTS that lasts for a day after their migraine and then goes away - this i thought was very telling.

Caffeine works short term for me but not long term.

[bjt22]

It could be a compensatory mechanism - or it could just be because our sympo systems are over excited? Until they understand migraines properly they might not know.

As for the comment about a whole body migraine - yeah i often feel exactly the same! Things that trigger migraines in people wiht migraines tend to trigger POTS symptoms in me. I also read of a small group of migraine patients have POTS that lasts for a day after their migraine and then goes away - this i thought was very telling.

Caffeine works short term for me but not long term.

There are some studies floating around out there that describe migraine as a sympathetic hypofunction. A transient autonomic failure. When I'm in migraine or cluster mode, they occur when my blood pressure and/or heart rate has dropped quickly. In fact, years and years ago, that was one of my first symptoms. I tried to explain that to doctors, but they looked at me as if I were speaking a different language!

My blood pressure drops ALL the time. I guess my question is for those like us, why does this sometimes lead to migraine and sometimes not? I suppose inflammatory response could have a lot to do with it. However, I walk around with what could be considered "aura" pretty much all the time.

[ramakentesh]

Yeah i have a pretty persistant aura as well - my doc told me this was from vasoconstriction from POTS - I always have visual snow and other visual defects, cant stand brihg tlights and have trouble tracking moving objects.

Whereas when i get a proper migraine i get horrid auras with paralysis and total visual distortions. scary.

[masumeh]

I looked up NO (nitric oxide) after reading your reply to the antioxidant post...some pages online mentioned that low NO results in vasocontriction. Could that be your issue? Maybe in that case, exercise would help (bc it boosts NO levels)?

Personally, I have lax veins and I think it's EDS related.

[ramakentesh]

Yeah there is that but then is the vasoconstriction of the head a result of blood pooling elsewhere? Perhaps stomach vasodilation causes peripheral vasoconstriction which leads to a greatly increased sympathetically mediated vasoconstriction or hypocapnia?

There are some supplements and amino acids that are potent increasers of neuronal nitric oxide. But since its still unclear whether I have an overall whole-body vasoconstriction or vasodilation in other places it wouldnt be safe for me to test these. It might help or it might make me much worse and its unclear to me at this stage which way it would go.

Time will tell I guess. i was thinking that targeted nitric oxide inhibators could actually be a good treatment for POTS - if they could make them specific for locations where pooling occurs.

Currently the only specific vasoconstrictors used in POTS are super expensive thus hard to get a prescription for.

[bjt22]

Ramakentesh,

I can give you a possibility that I think could explain some of what you are asking.

Let's accept that we have damage throughout the autonomic nervous system. It's a spotty damage...a little here, more there, and a bit more scattered in between. If we accept this, we can understand how function in many different systems would be effected. Now, let's assume that our bodies do what they always do, and try to compensate. There's a variety of mechanisms that would allow them to attempt to do so. We live with the effects every day. Don't forget, however, that the damage is not complete...it's most likely spotty. Those nerves that are still somewhat functional are probably getting massive amounts of hormonal and neural transmissions as our bodies signal to put out larger than normal amounts of these in an attempt to increase function. Let's go a step further...maybe we're not even capable of producing consistent amounts of these substances from day to day. Maybe most days, this is the case. Then on the unfortunate day that we put out normal amounts, what must that do to the still fairly normal parts of our nervous systems? What I'm describing could be termed a denervation hypersensitivity, and it explains a lot of the real mysteries that we seem to encounter. It explains the changing of our symptoms from day to day as well as the back and forth of the severity. Now, add onto this the fact that all of this might actually be leading to more damage on a regular basis. Everytime this happens, the whole compensation effort starts up again.

As to nitric oxide, well, I think the production of every natural substance in our bodies has been convulated due to dealing with the dysfunction. The NO connection could certainly explain one aspect, but I think we're in chicken-or-the-egg territory. It's very difficult to understand which came first.

[ramakentesh]

yeah your right and even if you swap the patchy nerve damage theory for endothelial cell dysfunction in specific places (as suggested in Dr Stewart's work) you could expect - if it behaves like other inflammatory disorders such as Rh. Arhritis, etc to wax and wane and be totally unpredictable.

And you make a good point - we are dealing with a fluid system that involved numerous chemicals and nerve activities and who knows what else.

[Guest tearose]

I think the whole inconsistent pattern IS due to the patches of damage in conflict with the patches of non-damage. Our bodies are trying to keep us in balance but the body response depends on what group of nerve fibers it samples to make the decisions!

tearose

[ramakentesh]

So your assuming that all patients with POTS have patchy nerve damage? Its possible and Dr Grubb I believe thinks that around 90% of POTS patients have this as a problem. It could explain a lot of the stuff we experience, but a simple vessel dilation problem could itself also explain POTS in my case. My hypersensativity to some medications has been interesting for me to. Although this seems to only relate to vasoactive medications for me (thank god as I need anti inflams for my ankylosing Spond).

But for me Id think that patchy nerve damage would yield pretty consistent results rather than results that improve and wax and wane constantly throughout the day and our lives.

Courses that wax and wane with spontaneous remissions and exacerbations are the hallmark of inflammatory disorders.

I dont accept that we have nerve damage in all cases. Clearly some POTS patients do - particularly those that exhibit pooling in their legs - but recent evidence is pointing to inflammation as a cause in POTS where the pooling is specific to the stomach area - as the link above suggests.