ramakentesh

Dont be fooled by random comments made by unknown people on wikipedia or random comments in some studies. The outcome of POTS in various patient groups and subdivisions based on primary etiology are completely unknown and unmeasured. There are no proper longtitudal studies. Remission is completely possible and Ive been told that spontaneous remission is definately possible. Over the years (ive had relapsing pots since 2003) ive noted that the patients that get POTS out of the blue and have one long bout that lasts two to five years seems to recover the best. the others are either sick all the time and variable or like me and relapse/remit with periods of almost complete wellness in between.

Worth a shot. problem is that small fibers, microvascular filtration and venous pooling occurs mostly in areas in the middle of the body rather than the cutaneous (skin) micro circulation.

I have small fiber neuropathy POTS and licorice was my main stay for years. Now it doesnt work as well but i have other mainstays.

Licorice is great. As well as its often reported blood volume increasing properties via sodium retention in the kidneys, it also acts as to increase cns dopamine, acts as a mild MAOI, can reduce nitric oxide in the endothelium (wish i could find that study again) and contains steroid-like compounds that can suppress autoimmunity.

Licorice is fantastic by the way. It contains natural steroid like compounds that can suppress autoimmunity, acts to increase dopamine in the brain which can help energy (is a mild central stimulant), reduces nitric oxide in the endothelium increasing vasoconstriction and ofcourse its main function is to trick the kidney into increasing sodium in the blood.

This is the nature of autoimmune and autoinflammatory illnesses. Very few other types of illnesses wax and wane with spontaneous flares and remissions. If you read patient descriptions of conditions like MS and Ankylosing Spondylitis you will note that their flares ups and remissions are identical. Id encourage anyone with random fluctuations in symptoms to see how they feel during the build up to a storm. Id also encourage anyone with this presentation to get a QSART or skin biospy as this presentation often occurs with neuropathic POTS (specifically the autoimmune small fiber autonomic neuropathy)

Im sceptical but good luck.

Hi I developed relapsing remitting Ankylosing spondylitis and POTS at the same time. In my case the pots side of things appears to be caused by small fiber autonomic neuropathy. There is a thought that most cases of secondary POTS with other systemic autoimmune disease may be small fiber related. Small fiber neuropathy and POTS in sarcoidosis completely resolved after a patient was put on humira, suggesting it may be cytokine inflammation of the small fibers. I was supposed to start simponi a while back but every time i go to start it my AS goes into complete remission for months on end. PM me if you want more details.

Reduced NE as in net deficiency - high then depletion.

Peripheral blood pressure measurements aren't very helpful with pots because usually patients are still exhibiting signs of reduced brain blood flow and faulty thoratic and stomach vasoconstriction. I would definitely avoid all hypotensive agents in dizzy pots unless you don't get dizzy. current evidence suggest lightheadedness in pots is caused by faulty alpha 1 adrenoceptor vasoconstricton - either from selective neuropathy, reduced NE or an autoimmune process. peripheral vasocobstriction may be compensatory - your body trying to help.

Of course you can take both. One is a peripheral alpha 1 agonist the other just makes you retain volume. blood pressure readings by arm cough are almost useless in pots. Pots is almost always about either regional or overall alpha 1 receptor failure or depletion of NE because of the faulty transporter. pots patients don't get symptoms caused by hypo or hypertension. They get symptoms similar to a hemorrhage - pooling in one location - usually the pelvis, stomach and chest where there may be small fiber neuropathy, alpha 1 receptor failure or reduced NE. The rest of the body and vasculature may be normal. the increased NE used to try and constrict struggling regions is felt full effect in the areas ( heart, arms, etc) where normal nervation and function is maintained resulting in the confusing profile of dizziness and weakness yet hyped up feelings and even elevated overall blood pressure. this applies if your a dizzy pots. in net deficiency some areas run out of NE while other areas can't clear it so again tachy, anxiety, inattention in brain and heart where tight synaptic cleft traps NE but pooling and dizziness caused by faulty vasocobstriction in the pelvis, stomach and chest where sympathetic synapses are wide and NE leaks away. many are on both midodrine and florinef including me.

http://www.ncbi.nlm.nih.gov/pubmed/23708963 Gastric emptying in postural tachycardia syndrome: a preliminary report http://www.ncbi.nlm.nih.gov/pubmed/23701223 Postural orthostatic tachycardia syndrome (POTS) in a child with type 1 diabetes

nearly all the recent studies on POTS suggest that blood pressure readings are not indicative of symptoms.

Here regarding QSART results of hyper v non hyper: http://www.ncbi.nlm.nih.gov/pubmed/20035362 Here in terms of NET deficiency/inhibition resulting in reduced orthostatic vasoconstriction and normal NE levels: http://www.ncbi.nlm.nih.gov/pubmed/18187607 http://www.ncbi.nlm.nih.gov/pubmed/19808400

These kinds of topics appear a lot. Most treatments are aimed at treating symptoms - if symptoms of excessive sympathetic drive are the major problem which can occur in all forms of POTS - then beta blockers may be helpful. This doesn't depend on whether your serum NE levels are below or above a certain number and increasingly the delineation of POTS that is being adopted is neuropathic v non neuropathic rather than hyper v non hyper because it MIGHT tell people more about the underlying etiology. The same number of hyper and non hyper POTS patients had QSART abnormalities meaning that some hyper and non hyper POTS patients may have the same underlying mechanism or cause. Some POTS patients have normal NE but its effects are potently potentiated, others have beta receptor super sensitivity - like some with EDS. Many patients with NET deficiency did not have overt 'hyperadrenergic' presentations. This was because it appeared that their vesicles ran out of norepinephrine, or alpha 2 receptors blunted NE release, or alpha 2 cerebral stimulatuion reduced sympathetic central outflow. So its murky.

Most POTS don't faint.

sounds reasonable. If you don't tolerate midodrine then phenylephrine is another option you can talk to your doc about.

Ive spent the last two months trying to work out how pseudoephedrine works so well for my POTS with limited success. A medication that tricks the body into releasing more norepinephrine would probably only work if something was stopping that NE from being released in the first place...

Dana - you and I have pretty darn similar POTS! Apparently some constituents in strong dark chocolate are hypotensive.

I deleted my POTS about Mayo because Ive spoken to a few people associated with them and I was being unfair. There are some there that 'theorise' that psychosomatic factors play a role in POTS but not that its behind the illness as they are big on the autoimmune small fiber neuropathy theory.

Is Dr Levine an expert in POTS?

Without wanting to sound annoying there is always doubt! Nothing about poorly understood conditions like POTS is ever unequivocal at least at the moment.

In hyper it would just add fuel to fire.

Sorry I meant if it makes the body shoot off too much NE where ne synthesis is compromised it may just make a person crash earlier.

Caffeine gives me a half hour boost and then a massive crash. It decrease adenosine modulation of sympathetic synaptic NE potentiation. It may also result in increased alpha 2 presumaptic receptor blunting on me release or cause the body to shoot off too much NE if synthesis is compromised. caffeine also reduces cerebral blood flow in normal people due to increased cerebralvascular resistance. for me it makes you think of net deficiency - boosted activity and release but then it all might leak into serum and bleed vesicles dry earlier.