Diary From A Research Patient At Vanderbilt

[ramakentesh]

did read the thread on BP and salt and think it is interesting. Apparently this thinking has been out there for many years. For me it causes me to question why salt helps instead of hurts since my body apparently produces too much adrenaline. Maybe it is the same way a stimulant works, if the drug produces it, my body gets to create less of it.???

The thinking is that perhaps POTS patients dont conserve salt balance correctly.

[kitt]

Rama,

Please share your research on this about 'POTS patients dont conserve salt balance correctly.'

I feel this may apply to me, but before I share my experience I'd be very interested in hearing what you've learned about this topic in your research. Thank you for sharing!

K

[Kellysavedbygrace]

Thanks much. Ronny, my son is recovering well. He has one more week of laying low but his appetite is back. Yeah!

Dr. Biaggioni did not say why the caffeine was helpful for some but he did say that many of the things that help us seem to be counterintuitive such as a high salt diet, caffeine and meds that stimulate the sympathetic nervous system.

Rama, is the sodium balance you are talking about measured by renin or Aldosterone?

[ramakentesh]

I was just thinking out aloud.

vand are interested in salt handling in a lot of their studies and it is interesting that even patients without low blood volume do better after saline. It makes you wonder - conditions where salt wasting occurs in the brain cause symptoms quite similar to POTS. it would be strange if perhaps the kidneys werent holding on to saly enough but it would be even weirder if the pial matter or the brain was not handling salt properly.

Dr. Biaggioni did not say why the caffeine was helpful for some but he did say that many of the things that help us seem to be counterintuitive such as a high salt diet, caffeine and meds that stimulate the sympathetic nervous system.

The statement above is quite interesting and in my case this is true. I know some researchers are testing hypothesis around whether cerebral autoregulation or cerebral vasomotor activity/vessel tone might be a primary problem in POTS rather than a secondary consequence. In that scenario the bodies overactive sympathetic system, tachycardia and vasoconstriction might all be a compensatory mechanism trying to maintain cerebral blood flow in the face of poor autoregulation or excessive vasoconstriction. All just conjecture on my part.

[Kellysavedbygrace]

Rama, what do you know about salt and it's role, if any in brain functioning? And why are you specifically thinking about the pia matter? Are you speculating that the sodium plays a role in creating inflammation somewhat like a case of meningitis?

[ramakentesh]

No sorry - I was just talking about sodium in general and about conditions where sodium is low having symptoms very similar to POTS. Saline for me is like heaven for 24 hours or so... i wish i could have it daily in some ways. florinef works ok but never as well for some reason (but in a normal body i feel it would).

What i have noticed is that weirdlyt when im potsie despite being on florinef my sweat off my head becomes super salty. when im feeling better florinef keeps the sodium level in my sweat to almost none. makes you wonder. But this is just my hunch.

As for the other issues that is theoretical. A paper by Julian Stewart mentioned excessive vasoconstriction in POTS being perhaps caused by mechanisms other than sympathetic excess as previously thought. it would make sense then that increasing sympathetic drive would benefit rather than worsen vasoconstriction if vasoconstriction was not caused by the sympathetic system in the first place.

In the past Blair Grubb and others have suggested that cerebral vasoconstriction in POTS is mediated by the sympathetic system. This might not take into account parasympathetic withdrawal which apparently occurs as a consequence of reduced stroke volume.

there are many studies that suggest that sympathetic input into cerebral blood flow is limited. Some suggest its controlled by parasympathetic innervation of pia matter. I am really warming to this theory but I dont think there is any evidence to support it yet.

[peregrine]

Are you referring to Julian Stewart's 2012 paper ("Mechanisms of Sympathetic Regulation in Orthostatic Intolerance")? I found that paper quite useful, particularly the data on how TTT responses are different in folks with POTS and folks with NMH/NCS that isn't an end consequence of POTS.

His theory on cerebral blood flow being largely independent of the sympathetic nervous system does help explain why, despite treatment with clonidine, my spaciness has not improved, while pretty much everything else - including classical SNS effects like sweating and overheating, and also fatigue that I ascribe to SNS overactivity - have mostly stopped happening to me, quite dramatically. Granted, I don't *know* that spaciness is due to cerebral blood flow issues (some parts of it, like always looking over my shoulder, becoming overstimulated, or starting more with sudden input, have also calmed somewhat with the clonidine - that hypervigilance-type behavior does go hand in hand with the SNS), but it does fit nicely into my personal mental model of how my POTS works.

To clarify, also, clonidine has helped somewhat with my seated/lying down cognitive impairment - I can now read papers for work! - but not with standing cognitive impairment; I still get flustered when I'm standing up. I'm wondering if perhaps it's helping indirectly via removing fatigue and distraction (if SNS overactivity is reduced, perhaps I am able to pay more attention to things/concentrate better when my brain already has enough blood due to sitting, whereas in the past I had enough blood, but had too much SNS activity and so couldn't focus), if it isn't having direct effects on cerebral blood flow? Who knows; no easy way to measure it without TCD, which seems to be not in general use anywhere, and certainly not for personal experiments like this! I do get cognitive impairment with clonidine at other times when seated/lying down, but it does correlate nicely with clonidine-induced low blood pressure - it makes good sense that one would have cognitive impairment when overall blood pressure is low.

Would you be willing to explain more about the parasympathetic innervation of pia matter idea? I haven't heard anything about it and am curious!

[ramakentesh]

Dr Stewart and Medow found that POTS patient's cerebral arteries do not vasodilate in response to stimuli. In the past this was associated with sympathetic drive but now they think its either to do with faulty vasomotor control of the cerebral blood vessels or abnormal cerebral autoregulation resulting in changes in brain blood flow synchronically with blood pressure variations (in other words loss of cerebral autoregulatory protection of perfusion). What effects autoregulation is unknown but parasympathetic withdrawal as a response to stroke volume might mess it up.

POTS patients also have abnormal critical venous collapse pressure.

[RichGotsPots]

Well i'm itching to read how their endothelium testing pans out.

Kelly, I really salute you. I've been thrown into the caregiver position before to, and it's so draining. Please get some rest and don't be afraid to ask friends and family for help, you deserve it!

[ashleighheath]

thank you for your beautiful diary entries. and your 2 corinthians translation.