jangle

Do they do mestinon?

Has anyone seen Dr. Sandroni at mayo Rochester? Will she prescribe treatments for pots?

I don't think pots is associated with brain lesions. I had a mri done in 2005 when my pots started that had no lesions and then again in 2011 which had no lesions. There's been no mention by any research group about pots causing brain lesions.

If the nerve damage was located in the hand, the neurologist probably forgot to warm the hand. POTS patients often have cold hands which can slow the conduction velocity on the oscilloscope, this can obscure the test. Also carpal tunnel syndrome could affect nerve conduction velocities in the hand.

Otherwise it's always a good idea to get a second opinion. Things like diabetes could cause some peripheral neuropathy that would show up on an EMG/NCS. Also things like Guillen-Barre Syndrome or AAG could potentially cause abnormal EEG findings. Low vitamin B-12 is a possibility, but one should probably get their B-12 levels measured before commencing a treatment and settling on that diagnosis. Ask your doctor about how to proceed.

Can you get saline infusions when you're having flares?

Ya low titer 1:80 speckled here.

I do believe if anyone can help it will be them. But I need to see the right people while I am there.

So I'm having an appointment at the Mayo Clinic In Rochester coming up. My biggest fear is going there just to have diagnostic testing done without much treatment recommendations. I've already gotten diagnosed with POTS at Baylor's autonomic center, so testing isn't going to be very helpful (they're just repeating the same tests over).

Since I'm beginning medical school soon, I really need a treatment regiment to help my presyncope and there are literally no doctors where I live who're willing to treat POTS.

What I'd like to do when I get to Mayo is bring out the list of medications:

-Octeotride

-EPO

-Mestinon

-Fludrocortisone

-Saline

-Possibly methylphenidate

-Ivabradine

The bolded medications are the ones I really want to try. But I guess I'm asking for advice on how to go about ensuring that I'm going to be given an opportunity for these treatments. Does anyone know who has been to Mayo before?

For anyone who has responded or knows someone who has responded to ivabradine, did it help the symptoms of presyncope?

That's great news. Excellent work and I hope the future brings even further achievement and improvement.

Your story seems similar to my own, I've had POTS now for 8 years and pretty much my remaining symptom is lightheadedness and dizziness. I would suggest getting referred to somewhere like Mayo or Vanderbilt - places that are doing research on POTS. I'm not sure about Cleveland clinic, but they're probably good too. Just don't expect your typical run of the mill doctor to know anything about POTS and/or be capable of treating it.

There are a host of treatments out there, that you may want to try. Please take a look 'round these forums, you'll see a lot of good advice.

I've seen publications recently about both these treatments being effective in treating POTS, but none of my doctors I believe have even heard of their use in POTS, and even if I brought them the studies I doubt they would consider it.

I know a few people on this forum have tried octeotride with success, but has anyone tried EPO?

That hypertension bothers me significantly, have you been tested for pheochromocytoma?

What are your symptoms? Do you feel dizzy, lightheaded etc?

Have your doctors suggested going to a place like vanderbilt or Mayo where they can do some vigorous testing as your case does not seem typical at all.

This is interesting - and it would be even more so if we could cross-reference with our data to verify a lack of a genetic defect. That would pretty much prove your idea that this is more epigenetic in nature.

In that light, maybe that is why anti-inflammatory drugs (steroids) prove helpful for some, which begs the question: Is the NET dysfunction for some/many of us secondary to some type of unknown autoimmune/inflammatory disorder or process?

Probably, but unfortunately the (clinical) research process is cold, rigid, and slow.

I am however excited that vanderbilt is behind this study, as before there really wasn't any major academic US institution pursuing NET - it's currently mostly being done in Australia.

Again, facing the options of treatment for such an autoimmune illness. It would probably be IVIG, as IVIG is the most reasonable treatment in an unreasonable environment.

Ideally, we'd be able to identify the specific autoantibody or cytokine, develop a specific drug that targets such thing, and utilize that.

http://dmm.biologists.org/content/early/2013/04/03/dmm.012203.abstract

They found that mice deficient in NET proteins was sufficient to produce the postural tachycardia with many of the associated symptoms.

In the majority of our cases, I don't think it's due to a genetic defect, but rather the epigenetic "switching off" of the expression of the gene - likely due to inflammatory factors. As found by Bayle's group.

Don't even get me started on the 'push your kids to pretend they are well' pseudoscience. The hypocrisy of their own paper suggesting physiological mechanisms and then - without any evidence whatsoever - that 'chronicity of symptoms is the result of patient somatic hypervigilence and symptom catastrophising'. I wonder if ms patients stopped thinking about their symptoms whether they would go away? Does neuropathy cure itself when ignored? Does aldosterone rise and cardiac mibg miraculously improve? perhaps diabetes patients should stop their insulin and avoid thinking about their disease? and ofcourse there is not one testable objective piece of evidence that can be measured that even supports the argument that pots has a psychogenic component other than the kids whose parents force them to pretend they are well.

The author who suggested hypervigilance and symptom catastrophising didn't know about the paper published by the other Mayo clinic group. When I was emailing him, he told me that there was only antibodies found against nerves in some POTS patients, when I showed him the study published by Mayo about autoantibodies to the heart, he got back to me saying that wasn't around at the time of his publication and he personally just had a conversation with Dr. Low who told him the role of those autoantibodies were unclear.

Anyways, this is interesting, but the only viable treatment for an ambiguous autoimmune disorder at this point would be IVIG or plasmapheresis.

Which IVIG isn't too bad, it's just expensive. Very expensive. If they have a clinical trial that pays for it, I'd be interested in joining it.

Heck, maybe I could start a clinical trial :D

You can ask your doctor about going to an academic clinic like mayo, Vanderbilt, or southwestern. Preferably the former 2 as mayo and Vanderbilt have dedicated autonomic specialists.

Since salt tabs help you might want to ask your doctor about florinef which helps you retain salt and water. Additionally ask your doctor about exercise as it can help a lot. Rows, jogging, stair master are all great tools that can relieve dizziness.

Good luck and best,

For the past 4 weeks I've been doing the stairmaster, and I've found it's been a lot more efficient at lowering my heart rate than simply jogging.

Before I started this last exercise regiment I tested my HR after 5 minutes of standing (still) I was in the 112-122 range (122 max)

Now I'm at 99-105 range after 5 minutes of standing, and I extended it to 6.5 minutes and it kept in that range.

Symptomatically I'm about the same, but I have had an increase in partial remission moments throughout the day.

Norepinephrine transporter inhibition is the only thing that consistently produces pots in healthy controls. Something to think about

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.

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.

Probably hyperventilation, you should try yoga type breathing exercises which actually train you to use less air.

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.

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.

Interesting direction:

http://jms.ndmctsgh.edu.tw/fdarticlee%5C3003127.pdf

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.