ramakentesh

All other types of neuropathy are permanent or long standing but small fiber neuropathy is different.

Sfn can definitely vary sporadically and wax and wane.

I think informed opinion and research-backed opinion is more valuable - respectfully - than patient hunches or speculative theories without research. Im not talking specifically about Lyme however. And when you say 'we' do you mean patients? or researchers? Sure, and part of that is the ability to critically analyse and reflect on the probability, reliability and research-basis for that information. A paper in a well-regarded peer-reviewed journal outweights the evidentiary basis of a random MD's opinion on a website. I just find it strange that new papers on the possible etiology of POTS are published constantly in medical journals like Hypertension and Circulation - some are hampered by selection bias, some by small cohorts and some by other issues, but they are peer-reviewed and the work is conducted by qualified and intelligent people, yet people on patient forums tend to largely ignore this stuff completely or talk about it as if it and speculative theories have the same validity or evidentiary basis. An example would be the recent CCSVI stuff going around in relation to POTS and Dysautonomia. There is ofcourse no research that even suggests that angioplastic procedures of the jugular veins has any effect on dysautonomias and the doctors involved can not provide any explanation of how it could benefit any of the suggested etiological mechanisms of POTS yet desperate people are desperate people... I dont completely discount any theory and i dont claim that science has yet revealed all the answers, but I also dont accept that the view that the conditions described in that website are definitively connected with POTS and i certainly dont believe that the majority of POTS patients have underlying Lyme disease.

cerebral hypoperfusion/presyncope.

Im probably repeating myself but I know personally at least two people that have COMPLETETY recovered from POTS. Both were sudden onset POTS and both worry about relapse. But both report that they are completely fine. Normally sudden onset POTS can resolve over time - some report three to five years. I have noticed there are those that have always had it, those that get it randomly and it stays, and those that get it randomly and wax and wane, and those that get it and it eventually goes away. that is the patterns ive noticed.

The causes of POTS in most cases are still unclear, poorly understood and hotly debated. There are also some patient-driven theories. There is somewhat of an interesting correlation between those with sudden onsets and either comorbid autoimmune conditions or small fiber neuropathy. Small fiber neuropathy in Sarcoidosis can follow a waxing and waning presentation and in diabetes and Sarcoidosis SFN with symptoms similar to POTS small fiber neuropathy has been demonstrated to suggest wider autonomic denervation (wider autonomic denervation has been demonstrated in these patients). However no one as yet has definitively demonstrated that small fiber neuropathy in POTS is definitive evidence of wider autonomic denervation of sympathetic fibers in veins and other locations. SFN is becoming increasingly commonly described as a complication in many autoimmune diseases, at least suggesting the possibility that it represents an autoimmune process. Some POTS patients with SFN have responded to IVIG which also supports this possibility. The other etiology with growing evidence is the acquired NET deficiency that Jangle was talking about.

if there is dizziness supressing NE might make the person feel worse.

What Alex says is accurate. In some POTS there can even be increased peripheral resistance but reduced thoratic/stomach vasoconstriction

Actually some of the 'hyper' symptoms can be caused by compensatory adrenalin/epinephrine release and beta receptor supersensitivity. When NE leaks into plasma as occurs perhaps in NET deficiency its lost to the body and its reception of it - unless its in a sympathetic synapse it has very little effect although there are beta receptors in other sites. When usually occurs is either the NE gets stuck in the synapse like in the heart and causes tachycardia or it may leak out of the synapse and stop further NE release from presynaptic vesicles causing vasodilation. Ofcourse in the brain its different. But Hyperadrenergic/Hyper POTS is just a description of the levels fo NE - I dont think it says anything helpful about the primary cause or etiology and sometimes it actually slaps a misnomer in relation to treatment on the condition - Hyper POTS can still have a neuropathic basis etc. Some docs recently have adopted the neuropathic v non neuropathic POTS delineation which I think is probably more helpful.

Ive noticed that many males tend to have moderate rises in postural blood pressure readings on standings. I have an increase in BP readings on standing but respond to BP boosting meds, rather than the opposite.

it messed my sleep up somehow for about four days actually - i remember that.

Yeah mestinon gave me a 20-30% improvement in dizziness with a calming general feeling of the sympathetic system. It can however combine with other meds like midodrine and phenylephrine. I had no adverse effects of any type. But I found after about 8-14 months its effects completely wore off and it did very little. Im sure after a rest it would work ok again. But Id say that vasoconstrictors are probably more helpful for me because they also give me energy - at least at the moment. I find it utterly bizarre that despite there being numerous acetylcholinesterase inhibitors available they are still mucking around trialling the one that someone found helped back in 2005-06...

I have noticed that abrupt onset tend to improve the best and quickest. Improvement usually occurs in this group.

What I tend to find is that patients often ignore peer reviewed science for the stuff that has very little research support and sometimes doesn't even follow basic fundamentals of physiology.

When you say that you have to know all the flare triggers, causes to make any progress don't you think your making an assumption about the validity of what your reading, its application to your situation and your ability to decipher the relevant peer reviewed science from the opinion and conjecture?

Simplistic was an accurate description. Also ignoring most of the science.

Its interesting - people with strong dynamic cerebral auto regulation can deal with profound reductions in orthostatic blood pressure whereas people with poor auto regulation can experience symptoms from even tiny reductions or so it seems. some with essential hypertension faint when Bp is normalized as well.

Sorry for typos - on phone

In most pots patients peripheral (arm) measurements of blood pressure nay not tell you that blood is polling in the stomach, legs or pelvis it that vasoconstriction in these regions is blunted, or that stroke volume us reduced, or that cerebral blood flow is reducing despite normal overall blood pressure or that cerebral auto regulation is locked to Bp fluctuations, etc. in my case I have mild orthostatic hypertension but medications that increase blood pressure make me feel better and nornalise my standing np. Others need yo suppress sympathetic drive to feel better.

Diets are good

I've never really thought that this theory explains many of the findings in CFS. Why would a cohort of CFS patients respond to ritixumab if it was merely all the result of cardiac insufficiency?

I think they are making assumptions about what they are measuring and what it indicates.

Dizziness is generally treated with florinef or pressors like midodrine or phenylephrine. I also find pseudoephedrine helpful.

Id comment but it would be medical advice so I wont

The treatment as I understand it is biofeedback based and based on the belief that POTS and NCS result purely from abnormalities in the balance of the sympathetic and parasympathetic nervous system. Those patients with very high tachycardia, sympathetic overactivity and parasympathetic problems may in theory benefit from these kinds of programs. there are others with underlying neuropathy or norepinephrine transporter deficiency that in my opinion might be afforded less benefit. Still people seem to report positive responses and while I am sceptical I wouldnt discourage anyone who could afford the price ($5,000) to consider it.