ramakentesh

At the moment its very high and I think this issue might relate to that.

I have noticed it seems potentially related to adrenergic surges as I am always having them significantly when it happens.

Thanks im on midodrine and beta blockers, I was on clonidine for a while but I gave it a rest due to increased fatigue.

Hi all - one of the new and very strange symptoms im getting at the moment is this feeling where as soon as I dose I fall straight into an utterly bizarre dream with random things going on or my leg will twitch and ill jolt wide awake. This goes all night and is accompanied by continual adrenalin surges. Anyone relate? Thanks

Yeah that sounds very similar to what i experience.

Sounds horrid. Sorry you are experiencing that.

You noticed any itching with the SFN? That and not being able to tell cold from hot on my feet were the reasons I got that biopsy done. I was positive but years later i was negative and POTS was the same so work that out

I thought about this for OCD that I acquired during the pandemic to a degree but yeah unfortunately with the POTS brain who knows what it might do - might go great, might be a two month crash.

Yes there does seem to be a connection - what neurological symptoms do you think are being caused by APS?

My POTS over the years has literally come and gone at the drop of a hat sometimes - once i drank a lemonade in a crash and immediately felt fantastic. I bought lots more of that lemonade but sadly it never happened again

Interestingly after ten years of having what i would describe loosely as 'zombie POTS' where i just felt terrible OI and dizziness, fatigue etc which responded quite well to midodrine and florinef, last year my POTS did a complete 180 degrees and hit me with the most intense hyperadrenergia ive ever experienced in 18 years of POTS on and off. It went on for 6 and then 15 days of solid daily BPs of 180/110 and HRs of 140 and it was utterly horrendous. I was climbing the walls and actually felt like I was mentally losing it from the constant feeling of panic. And I have absolutely no idea why it went that way after over a decade of a fairly stable presentation with relapses and remissions. Pretty much threw out all of the past research I had read about the causes of POTS - made me start to think it may be more of a spectrum or something; or perhaps sometimes it just swings the other way for what ever reason. So now Im on clonidine and its been very helpful for me although it promotes OI but I kind of prefer dizziness to feeling so wired I cannot sleep and startle all day at birds etc.

Sorry to hear its come back but it does seem to have a habit of doing that during periods of change or hormonal fluctuations. Jealous of 10 year remissions however

All etiologies of POTS can display 'hyperadrenergic' features. Neuropathic POTS patients can display these features. POTS patients with low-flow POTS and elevated Angiotensin II would meet the definition of Hyperadrenergic POTS. The patients in the adrenergic autoantibody studies with the highest titers for alpha receptor antibodies had hyperadrenergic features. The same amount of 'Hyperadrenergic' as 'neuropathic' POTS patients had small fiber neuropathy suggesting the possibility of a common primary etiology. This is why several docs including Dr Raj arent super keen on people 'subtyping' a group of disorders with unclear etiologies. All of this suggests that there is no fixed medical consensus on the etiology of 'Hyperadrenergic POTS' as a distinct diagnosis or pathology and that it is a presentation. Lastly - as an aside, Norepinephrine and adrenalin are different. This is important because hyperadrenergic POTS patients generally have elevated norepinephrine (which is preferential for alpha 1 and alpha 2 adrenergic receptors) rather than epinephrine (which is preferential for beta 1 and beta 2 adrenergic receptors).

The excessive sympathetic response to standing hypothesis is interesting because vesicles in sympathetic synapses rely heavily on reuptake for norepinephrine stores - meaning if there was a lack of transporter the vesicle would be completely depleted of norepinphrine without an increase to tyrosine hydroxylase. This would potentially result in hypotension. This is further evidenced by NET inhibition in heathy people which increases standing heart rate, impaited baroreflex sensitivity but not a hyperadrenergic state. The angiotensin ii low flow crowd did have a true hyperadrenergic response yet vasodilators made them feel worse. I really beleive that proper hyperadrenergic POTS - if if is more than a presentation - is probably mediated by central processes

Ive had small fiber neuropathy diagnosed twice. Other than itching and not being able to tell temperature in my feet luckily i had no other symptoms.